scholarly journals Levels of cytokines in extended purulent peritonitis and methods of immunocorrection

2020 ◽  
Vol 87 (11-12) ◽  
pp. 54-61
Author(s):  
E. T. Mammadova
Keyword(s):  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Basic Therapy ◽  
Tnf Α ◽  
Purulent Peritonitis ◽  
Treatment Measures ◽  
Healthy Persons ◽  
Basic Treatment ◽  
Cytokines Secretion ◽  
Severity Degree

Objective. Comparative studying of the cytokines secretion dynamics in extended purulent peritonitis in postoperative period on background of the standard basic therapy and its combination with cytokinotherapy. Materials and methods. The levels of anti-inflammatory cytokines IL-2, IL-6, IL-8 and TNF-α in the blood of 97 patients, suffering extended purulent peritonitis of various genesis and various severity degree, were determined. Depending on kind of therapy conducted, the patients were divided into two Groups: the first one - 52 patients, obtaining standard basic therapy and the second - 45 patients, to whom cytokinotherapy was prescribed additionally to standard basic therapy. Results. In the Group II patients the levels of IL-2, IL-6, IL-8 and TNF-α were raised significantly in reactive phase in 2.1 (p=0.035), 2.4 (p=0.002), 2.0 (p=0.004) and 3.5 (p=0.001) times, accordingly; toxic - in 5.1 (p<0.001), 5.6 (p<0.001), 2.4 (p<0.001) and 6.6 (p<0.001) times, accordingly; terminal - in 8.7 (p<0.001), 8.7 (p<0.001), 4.7 (p<0.001) and 8.6 (p<0.001) times, accordingly, comparing with control. On the tenth postoperative day the concentration of proinflammatory cytokines have lowered significantly in comparison to preoperative data. Conclusion. In all the patients, owing various degrees of the extended purulent peritonitis severity, preoperatively a statistically significant raise of concentration of proinflammatory cytokines IL-2, IL-6, IL-8 and TNF-­α, comparing with indices in healthy persons, was noted. Targeted immunocorrection, using combined cytokinotherapy on background of complex basic treatment measures, normalizes a cytokinic balance.

scholarly journals Plasma levels of melatonin, certain cytokines and placental growth factor at non-pharmacological correction of pineal function in pregnant women with intrauterine growth restriction

2020 ◽  
Vol 8 (2) ◽  
Author(s):  
A. Berbets ◽  
Keyword(s):  
Immune System ◽  
Growth Factor ◽  
Pineal Gland ◽  
Pregnant Women ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Placental Growth Factor ◽  
Placental Insufficiency ◽  
Tnf Α ◽  
Anti Inflammatory

The pineal gland produces the important hormone melatonin, the level of which in the blood of pregnant women decreases in case of placental insufficiency. The effect of dysfunction of the pineal gland on the immune system of pregnant women and on the angiogenic activity of the placenta during pregnancy remains insufficiently studied. Objective: to establish the effect of our method of non-drug correction of function of pineal gland on the state of the cytokine part of the immune system and on the synthesis of placental growth factor (PlGF) in pregnant women with placental insufficiency manifesting as fetal intrauterine growth restriction (IUGR). Material and methods. 46 pregnant women with IUGR at 30-36 weeks of gestation were examined. The group was divided into two subgroups: with non-drug correction of the pineal gland function (n = 25) and without correction (n = 21). The method of correction included a set of measures of following of lighting regimen, activity and sleep for 14 days. The control group consisted of 20 women with uncomplicated pregnancy. Levels of melatonin, PlGF, TNF-α, IL-1β, IL-6, IL-4, IL-10 were determined in the venous blood by enzyme-linked immunosorbent assay. Results. It was established that the concentration of melatonin in the blood of pregnant women with IUGR was significantly reduced, as well as the concentration of PlGF (p < 0.01). Significant changes were also found in pregnant women with placental insufficiency, namely, increased concentrations of proinflammatory cytokines, such as TNF-α (p < 0.05), IL-1-β (p < 0.001) and IL-6 (p < 0.05), comparing to healthy pregnant women. Also, in the group of pregnant women with IUGR the levels of anti-inflammatory cytokines IL-4 (p <0.001) and IL-10 (p < 0.001) were elevated in comparison to the control group. After application of the developed complex of non-drug correction of pineal gland function, the concentration of melatonin in the blood of pregnant women in the subgroup of correction increased significantly, comparing to the subgroup without correction (p < 0.001), as well as the level of PlGF (p < 0.05). Also, significantly lower levels of proinflammatory cytokines TNF-α, IL-1-β and IL-6 were observed in pregnant women in the subgroup of correction (p < 0.01). Regarding anti-inflammatory cytokines, under the influence of the developed complex of measures there was a decrease in the level of IL-4 and an increase in the level of IL-10 (p < 0.01). Conclusions. When the measures, aimed at non-drug correction of function of pineal gland, are applied in pregnant women with placental insufficiency, manifested as IUGR, the following changes are observed: increased of plasma levels of melatonin and placental growth factor, decreased of levels of proinflammatory cytokines. We suggest that the pineal gland exerts its effect on the immune system through melatonin, which moderates the activity of pro- and anti-inflammatory cytokines, thereby reducing the influence of inflammation on placental tissue, what results in increasing of concentrations of placental growth factor in the blood of pregnant women.

scholarly journals Cytokines in the blood of patients with type 2 diabetes mellitus depending on the level of overweight/obesity (literature review and own data)

2021 ◽  
Vol 17 (7) ◽  
pp. 534-551
Author(s):  
K.P. Zak ◽  
V.V. Popova ◽  
V.L. Orlenko ◽  
O.V. Furmanova ◽  
N.D. Tronko
Keyword(s):  
Type 2 Diabetes ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Peripheral Blood ◽  
Control Group ◽  
Obese Women ◽  
Cytokine Network ◽  
Tnf Α ◽  
Anti Inflammatory

The paper analyzes the current literature data and the results of our own researches concerning the state of the cytokine network: pro- and anti-inflammatory cytokines (interleukin (IL) 1α, IL-1β, IL-4, IL-6, IL-10, IL-17 and tumor necrosis factor (TNF) α), α- and β-chemokines, including IL-8 and IL-16, as well as adipokines (leptin and adiponectin) in the peripheral blood of patients with type 2 diabetes (T2D) with normal and increased body weight/obesity. It has been shown that patients with T2D are cha­racterized by an increased content of proinflammatory cytokines (IL-1, IL-6, IL-17, TNFα), α- and β-chemokines in the peripheral blood, including IL-8 and IL-16, as well as leptin with a decrease in adiponectin content. In lean patients (with body mass index (BMI) < 25.5 kg/m2) compared to lean normoglycemic individuals from the control group (BMI < 25.5 kg/m2), there is a small but significant increase in IL-1β, IL-6, IL-17, TNFα and leptin, which, as BMI increases, significantly increases in severe obesity (BMI > 30.0 kg/m2), especially in obese women (BMI > 35.0 kg/m2). Similarly, an increase in proinflammatory cytokines is observed in normoglycemic people, but not as signifi­cant as in T2D. Less clear data were obtained when during determination of the anti-inflammatory cytokines IL-4 and IL-10, which is explained by a significant polymorphism of their genes, and both protective and compensatory effects on pro-inflammatory cytokine rise. In T2D patients, especially those with obesity, there is an increase in the leptin level and a decrease in the adiponectin content. The severity of the course and the percentage of mortality are closely associated with the BMI of patients. The effectiveness of the fight against an increase in the incidence of T2D should be primarily aimed at preventing obesity, and in case of already developed T2D — at reducing concomitant obesity. The analysis of the data presented also suggests that a sharp increase in the content of pro-inflammatory cytokines (so called cytokine storm) observed in patients with T2D and obesity infected with COVID-19, is a consequence of the summation and potentiation of already existing inflammatory process.

scholarly journals Expression of proinflammatory cytokines in stable angina

2013 ◽  
Vol 4 (1) ◽  
pp. 20-23
Author(s):  
A. N Zakirova ◽  
N. E Zakirova
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Functional Class ◽  
Control Group ◽  
Moderate Increase ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Tnf Α ◽  
Healthy Persons ◽  
Pro Inflammatory Cytokines

Objective: to evaluate the severity of immuno-inflammatory responses under stable stenocardia in patients with ischemic heart disease (IHD). Patients and intervention: the study included 83 patients suffering from IHD. Among them 30 cases were diagnosed as functional class (FC)-II stenocardia, 27 cases as FC-III stenocardia and 26 cases as FC-IV stenocardia. The control group included 25 healthy persons. For characterizing the immuno-inflammatory responses we examined the level of C-reactive protein (CRP), pro-inflammatory (IL-1b, IL-6, TNF-α) and anti-inflammatory (IL-4, IL-10) cytokines by the immunoenzymic procedure. Results: FC-II stenocardia showed normal levels of CRP and pro-inflammatory cytokines. FC-III stenocardia was associated with a moderate increase in markers of an inflammation. FC-IV stenocardia was characterized by maximum levels of CRP and pro-inflammatory cytokines. Conclusion. The intensity of immuno-inflammatory responses depends on more or less serious course of stenocardia in patients with IHD.

scholarly journals Secretion of proinflammatory cytokines by normal human melanocytes in response to lipopolysaccharide.

2011 ◽  
Vol 58 (4) ◽  
Author(s):  
Irena Tam ◽  
Krystyna Stępień
Keyword(s):  
Immune System ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Large Body ◽  
Dependent Manner ◽  
Skin Immune System ◽  
Human Melanocytes ◽  
Tnf Α ◽  
Normal Human ◽  
Dose Dependent

A large body of evidence suggests that epidermal melanocytes are an integral part of the skin immune system and can be considered immunocompetent cells. Recently, it has been reported that human melanocytes constitutively express Toll-like receptors and may be involved in the induction of several inflammatory cytokines. In the study the secretion of IL-1β, IL-6 and TNF-α by cultured normal melanocytes was investigated after stimulation with lipopolysaccharide. LPS increased the secretion of IL-1β in a dose-dependent manner. IL-1β stimulated release of IL-6 and TNF-α by melanocytes, whereas LPS activated production of TNF-α, but not of IL-6. These observations indicate that LPS can participate in the regulation of cytokine activity in normal human melanocytes and suggest that cytokines released by melanocytes could affect melanocytes themselves or/and other cells of the epidermis.

Hydrolyzed Fish Collagen Inhibits Inflammatory Cytokines Secretion in Lipopolysaccharide-Induced HUVECs

2014 ◽  
Vol 1025-1026 ◽  
pp. 570-573 ◽  
Author(s):  
Chao Liu ◽  
Yang Xue ◽  
Jiao Sun
Keyword(s):  
Inflammatory Cytokines ◽  
Cytokine Production ◽  
Umbilical Vein ◽  
Promising Candidate ◽  
Tnf Α ◽  
Fish Collagen ◽  
Anti Inflammatory ◽  
Umbilical Vein Endothelial Cells ◽  
Cytokines Secretion

The present study was designed to investigate the effects of hydrolyzed fish collagen (HFC) on the cytokine production of lipopolysaccharide (LPS)-induced human umbilical vein endothelial cells (HUVECs). The in vitro inflammation model was established using LPS-induced HUVECs.The cell viability of HUVECs and the secretion level of inflammatory cytokines,IL-6, IL-8, and TNF-α from LPS-treated HUVECs exposed to HFC were determined respectively using MTT and ELISA assays. Our results indicate that HFC promoted HUVECs proliferation, and significantly reduced IL-6, IL-8, and TNF-α production in LPS-stimulated HUVECs. It suggested that HFC had a prominent anti-inflammatory property, HFC could be considered as a promising candidate for anti-inflammatory wound dressing.

Anti-Inflammatory Effects of Moxifloxacin with and without Anti Toll-Like Receptors and Protein-Tyrosine-Kinase Inhibitors in Human Monocytes Stimulated with Aspergillus fumigatus.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4217-4217
Author(s):  
Ina Fabian ◽  
Avital Levitov ◽  
Debby Haite ◽  
Drora Halperin ◽  
Jacob Romano ◽  
...  
Keyword(s):  
Invasive Aspergillosis ◽  
Aspergillus Fumigatus ◽  
Proinflammatory Cytokines ◽  
Autologous Serum ◽  
Dependent Manner ◽  
Protein Tyrosine ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Dose Dependent ◽  
Cytokines Secretion

Abstract Invasive aspergillosis is a life-threatening disease in immunocompromised patients. Studies have shown that conidia from Aspergillus fumigatus (AF) induce the release of proinflammatory cytokines from leukocytes and provoke an inflammatory response. Although cytokines such as TNF-α and IL-8 are critical for optimal host defenses, in some patients with invasive aspergillosis such as patients with neutropenia or allergic bronchopulmonary aspergillosis, limiting the immune response by decreasing cytokine release could prove beneficial. We have shown that the fluoroquinolone moxifloxacin (MXF) conferred protective anti-inflammatory effects in a murine model of Candida pneumonia in immune suppressed animals (AAC46: 2442, 2002). In the present study, we investigated the effect of MXF on cytokine response and signal transduction mechanisms in human peripheral blood monocytes (PBMN) of healthy individuals stimulated with conidia of AF. PBMN incubated with 2% autologous serum were stimulated for 6 h with AF (1.5x106/ml) and cytokine secretion was measured with and without the addition of MXF. Secretion of IL-8, IL-1β and TNF-α was significantly enhanced by AF (4.3, 8.2 and 7-fold respectively), while MXF (5–20μg/ml) inhibited the cytokines secretion in a dose dependent manner up to 46%, 72% and 73% respectively (p&lt;0.05). Recognition of invading microorganisms by the innate immune system is a first step in their successful elimination. In the mouse, toll-like receptor (TLR) 2 and 4 were found to be essential for AF-induced activation of macrophages while conflicting data have been published regarding human macrophages. We treated PBMN with blocking antibodies (Ab) directed against TLR2 and TLR4 and found that both TLRs are involved in cellular sensing of AF. Blocking of PBMN with a combination of anti-TLR2 and 4 Ab before exposure to AF resulted in 42%, 46% and 61% decrease in IL-8, IL-1β and TNF-α, secretion, respectively. Pre-incubation of the cells with MXF (20 μg/ml) and the combined anti-TLR2 and 4 Ab resulted in an additional decrease in the cytokines secretion up to 60%, 68% and 80%, respectively. Previous studies have implicated activation of protein tyrosine kinases (PTK) in LPS-induced NFkB activation and TNF-α production. In-vitro studies performed previously by us showed that MXF inhibits NFkB and MAPK activation and the synthesis of proinflammatory cytokines in activated human monocytic cells (AAC48:1974, 2004). In the present study we stimulated PBMN with AF, with and without the PTK inhibitor, genistein (Gen) in the presence and absence of MXF. Gen (5–40 μM) inhibited in a dose dependent manner IL-8 secretion up to 25%. Pre-incubation of PBMN with MXF (20 μg/ml) and Gen resulted in an additional decrease in IL-8 secretion up to 49%. Our results indicate that the anti-inflammatory effect of MXF in AF-stimulated PBMN does not signal via TLR2 or TLR4, nor via PTK. Further studies in invasive aspergillosis models are needed to evaluate the importance of these immunomodulatory effects.

Evaluation of the cytokin status of women with miscarriage

2019 ◽  
pp. 59-63
Author(s):  
N. Skrypchenko ◽  
◽  
I. Vorobyova ◽  
T. Mazur ◽  
V. Tkachenko ◽  
...  
Keyword(s):  
Immune Response ◽  
Pregnant Women ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Cervical Mucus ◽  
Enzyme Analysis ◽  
Control Group ◽  
Inflammatory Reactions ◽  
Tnf Α ◽  
Anti Inflammatory

During pregnancy, a unique new equilibrium state appears between the systems of the specific and nonspecific mothers immunity. Besides, the cytokine cascade is launched, which includes proinflammatory and anti-inflammatory factors of influence. The balance between these two groups of mediators determines the nature of the course and outcome of the gestation process. The objective: to determine the role of mediators of pro-inflammatory and anti-inflammatory reactions of gestation intercourse in patients with miscarriage. Materials and methods. The main group (the first group) was made up of 153 pregnant women with miscarriage. The control group (the second group) consisted of 25 relatively healthy women with a physiological course of pregnancy and a complcated obstetric and gynecological anamnesis, with one and more physiological births in anamnesis. The concentration of cytokines IL-1 β, IL-6, IL-8, IL-10, TNF- α in the blood and their content in cervical mucus by solid-phase immune-enzyme analysis was determined. Results. Consequences of previous pregnancies having a background of inflammatory complications of genital and extragenital genesis create conditions for long-term persistence of latent infection, including in the uterine cavity and cervical canal, followed by infection of the fetus, and contribute to the development of immune imbalance during gestation, which leads to a cascade of homeostasis disorders with the development of complications of the pregnancy intercourse and perinatal pathology. Thus, the presence of clinical symptoms of the threat of premature abortion occurs in the context of an increase in the concentration of proinflammatory cytokines (IL-6, IL-8, TNF- α and IL-1 β) in serum.Reducing the concentration of IL-10 in non-pregnant women, relative to such in control group, throughout the entire pregnancy in the blood and its content in cervical mucus indicates a violation of the balance of pro– and anti-inflammatory cytokines in the direction of pro-inflammatory reactions and violation of the local immune response. Conclusions. In women with a loss in the first trimester there is a pro-inflammatory activity of the immune response, which is an important pathogenetic factor in the development of abortion in different gestational periods. Key words: miscarriage, proinflammatory cytokines, anti-inflammatory cytokines.

scholarly journals Brain-Derived Neurotrophic Factor Suppressed Proinflammatory Cytokines Secretion and Enhanced MicroRNA(miR)-3168 Expression in Macrophages

2022 ◽  
Vol 23 (1) ◽  
pp. 570
Author(s):  
Hui-Chun Yu ◽  
Hsien-Bin Huang ◽  
Hsien-Yu Huang Tseng ◽  
Ming-Chi Lu
Keyword(s):  
Proinflammatory Cytokines ◽  
Neurotrophic Factor ◽  
Human Monocyte ◽  
Brain Derived Neurotrophic Factor ◽  
Neurotrophin Receptor ◽  
Enzyme Linked Immunosorbent Assay ◽  
P75 Neurotrophin Receptor ◽  
Tnf Α ◽  
Potential Strategy ◽  
Cytokines Secretion

We investigated the role of brain-derived neurotrophic factor (BDNF) and its signaling pathway in the proinflammatory cytokines production of macrophages. The effects of different concentrations of BDNF on proinflammatory cytokines expression and secretion in U937 cell-differentiated macrophages, and human monocyte-derived macrophages were analyzed using enzyme-linked immunosorbent assay and real-time polymerase chain reaction. The CRISPR-Cas9 system was used to knockout p75 neurotrophin receptor (p75NTR), one of the BDNF receptors. Next-generation sequencing (NGS) was conducted to search for BDNF-regulated microRNA. A very low concentration of BDNF (1 ng/mL) could suppress the secretion of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-6 in lipopolysaccharide (LPS)-stimulated macrophages but did not change their mRNA expression. BDNF suppressed IL-1β and IL-6 secretion in human monocyte-derived macrophages. In U937 cells, BDNF suppressed the phosphorylation of JNK and c-Jun. The p75NTR knockout strongly suppressed IL-1β, IL-6, and TNF-α secretion in macrophages and LPS-stimulated macrophages. BDNF regulated the expression of miR-3168 with Ras-related protein Rab-11A as its target. In conclusion, BDNF suppressed proinflammatory cytokines secretion in macrophages and inhibited the phosphorylation of JNK. Knockout of p75NTR suppressed proinflammatory cytokines expression and secretion. BDNF upregulated the expression of miR-3168. The inhibition of p75NTR could be a potential strategy to control inflammation.

scholarly journals Accelerated Prion Disease in the Absence of Interleukin-10

2004 ◽  
Vol 78 (24) ◽  
pp. 13697-13707 ◽  
Author(s):  
Alana M. Thackray ◽  
Andrew N. McKenzie ◽  
Michael A. Klein ◽  
Angus Lauder ◽  
Raymond Bujdoso
Keyword(s):  
Inflammatory Cytokines ◽  
Prion Disease ◽  
Proinflammatory Cytokines ◽  
Incubation Time ◽  
Transforming Growth Factor ◽  
Cytokine Gene Expression ◽  
Wild Type ◽  
Terminal Disease ◽  
Tnf Α ◽  
Anti Inflammatory

ABSTRACT The identity of pro- and anti-inflammatory cytokines in the neuropathogenesis of prion diseases remains undefined. Here we have investigated the role of anti-inflammatory cytokines on the progression of prion disease through the use of mice that lack interleukin-4 (IL-4), IL-10, IL-13, or both IL-4 and IL-13. Collectively our data show that among these anti-inflammatory cytokines, IL-10 plays a prominent role in the regulation of prion disease. Mice deficient in IL-10 are highly susceptible to the development of prion disease and show a markedly shortened incubation time. In addition, we have correlated cytokine gene expression in prion-inoculated IL-10−/− mice to wild-type-inoculated animals. Our experiments show that in the absence of IL-10 there is an early expression of tumor necrosis factor alpha (TNF-α). In wild-type prion-inoculated mice, the expression of TNF-α mRNA occurs at a later time point that correlates with the extended incubation time for terminal disease development in these animals compared to those that lack IL-10. Elevated levels of IL-13 mRNA are found at early time points in the central nervous system of prion-inoculated IL-10−/− mice. At terminal disease, the brains of wild-type mice inoculated with RML or ME7 are characterized by elevated levels of mRNA for the proinflammatory cytokines TNF-α and IL-1β, together with the anti-inflammatory cytokines IL-10, IL-13, and transforming growth factor beta. Our data are consistent with a role for proinflammatory cytokines in the initiation of pathology during prion disease and an attempt by anti-inflammatory cytokines to regulate the ensuing, invariably fatal pathology.

scholarly journals Endogenous Pro- and Anti-Inflammatory Cytokines Differentially Regulate an In Vivo Humoral Response to Streptococcus pneumoniae

2002 ◽  
Vol 70 (2) ◽  
pp. 749-761 ◽  
Author(s):  
Abdul Q. Khan ◽  
Yi Shen ◽  
Zheng-Qi Wu ◽  
Thomas A. Wynn ◽  
Clifford M. Snapper
Keyword(s):  
Streptococcus Pneumoniae ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Humoral Response ◽  
Lymphoid Cells ◽  
Primary Immunization ◽  
Tnf Α ◽  
Ifn Γ ◽  
Anti Inflammatory

ABSTRACT Proinflammatory cytokines play a critical role in innate host defense against extracellular bacteria. However, little is known regarding the effects of these cytokines on the adaptive humoral response. Mice injected with a neutralizing anti-tumor necrosis factor alpha (TNF-α) monoclonal antibody (MAb) at the time of primary immunization with intact Streptococcus pneumoniae (strain R36A) showed a substantial reduction in both the primary immunoglobulin G (IgG) response specific for the cell wall protein, pneumococcal surface protein A (PspA), as well as in the development of PspA-specific memory. In contrast, anti-TNF-α MAb injected only at the time of secondary immunization with R36A failed to alter the boosted anti-PspA response. TNF-α was required only within the first 48 to 72 h after primary immunization with R36A and was induced both by non-B and non-T cells and by lymphoid cells, within 2 to 6 h after immunization, with levels returning to normal by 24 h. Thus, the early innate release of TNF-α was critical for optimal stimulation of the subsequent adaptive humoral response to R36A. Additional proinflammatory (interleukin 1 [IL-1], IL-6, IL-12, and gamma interferon [IFN-γ]) as well as anti-inflammatory (IL-4 and IL-10) cytokines were also transiently induced. Mice genetically deficient in IL-6, IFN-γ, or IL-12 also showed a reduced IgG anti-PspA response of all IgG isotypes. In contrast, IL-4−/− and IL-10−/− mice immunized with R36A showed a significant elevation in the IgG anti-PspA response, except that there was decreased IgG1 in IL-4−/− mice. In this regard, a marked enhancement in the induction of proinflammatory cytokines was observed in the absence of IL-10, relative to controls. Ig isotype titers specific for the phosphorycholine determinant of C-polysaccharide were similarly regulated, but to a much more modest degree. These data suggest that proinflammatory and anti-inflammatory cytokines differentially regulate an in vivo protein- and polysaccharide-specific Ig response to an extracellular bacteria.

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