scholarly journals Effect of Anatomical Distribution of Mast Cells on Their Defense Function against Bacterial Infections

2003 ◽  
Vol 197 (11) ◽  
pp. 1417-1425 ◽  
Author(s):  
Tomoko Jippo ◽  
Eiichi Morii ◽  
Akihiko Ito ◽  
Yukihiko Kitamura
Keyword(s):  
Survival Rate ◽  
Mast Cells ◽  
Peritoneal Cavity ◽  
Bacterial Infections ◽  
Poor Survival ◽  
Anatomical Distribution ◽  
Neutrophil Influx ◽  
Bacterial Peritonitis ◽  
Tnf Α ◽  
Defense Function

Mast cells were depleted in the peritoneal cavity of WBB6F1-tg/tg mice that did not express a transcription factor, MITF. When acute bacterial peritonitis was induced in WBB6F1-+/+, WBB6F1-W/Wv, and WBB6F1-tg/tg mice, the proportion of surviving WBB6F1-+/+ mice was significantly higher than that of surviving WBB6F1-W/Wv or WBB6F1-tg/tg mice. The poor survival of WBB6F1-W/Wv and WBB6F1-tg/tg mice was attributed to the deficient influx of neutrophils into the peritoneal cavity. The injection of cultured mast cells (CMCs) derived from WBB6F1-+/+ mice normalized the neutrophil influx and reduced survival rate in WBB6F1-W/Wv mice, but not in WBB6F1-tg/tg mice. This was not attributable to a defect of neutrophils because injection of TNF-α increased the neutrophil influx and survival rate in both WBB6F1-W/Wv and WBB6F1-tg/tg mice. Although WBB6F1-+/+ CMCs injection normalized the number of mast cells in both the peritoneal cavity and mesentery of WBB6F1-W/Wv mice, it normalized the number of mast cells only in the peritoneal cavity of WBB6F1-tg/tg mice. Mast cells within the mesentery or mast cells in the vicinity of blood vessels appeared to play an important role against the acute bacterial peritonitis. WBB6F1-tg/tg mice may be useful for studying the effect of anatomical distribution of mast cells on their antiseptic function.

scholarly journals Febrile Core Temperature Is Essential for Optimal Host Defense in Bacterial Peritonitis

2000 ◽  
Vol 68 (3) ◽  
pp. 1265-1270 ◽  
Author(s):  
Qinqqi Jiang ◽  
Alan S. Cross ◽  
Ishwar S. Singh ◽  
T. Timothy Chen ◽  
Rose M. Viscardi ◽  
...  
Keyword(s):  
Core Temperature ◽  
Host Defense ◽  
Bacterial Infections ◽  
Bacterial Load ◽  
Cytokine Expression ◽  
Microbial Pathogens ◽  
Necrosis Factor Alpha ◽  
Bacterial Peritonitis ◽  
Tnf Α ◽  
Factor Alpha

ABSTRACT Fever, a nonspecific acute-phase response, has been associated with improved survival and shortened disease duration in infections, but the mechanisms of these beneficial responses are poorly understood. We previously reported that increasing core temperature of bacterial endotoxin (LPS)-challenged mice to the normal febrile range modified expression of tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), and IL-6, three cytokines critical to mounting an initial defense against microbial pathogens, but survival was not improved in the warmer animals. We speculated that our inability to show a survival benefit of optimized cytokine expression in the warmer animals reflected our use of LPS, a nonreplicating agonist, rather than an infection with viable pathogens. The objective of this study was to determine if increasing murine core temperature altered cytokine expression and improved survival in an experimental bacterial peritonitis model. We showed that housing mice at 35.5°C rather than 23°C increased core temperature from 36.5 to 37.5°C to 39.2 to 39.7°C, suppressed plasma TNF-α expression for the initial 48 h, delayed gamma interferon expression, improved survival, and reduced the bacterial load in mice infected with Klebsiella pneumoniae peritonitis. We showed that the reduced bacterial load was not caused by a direct effect on bacterial proliferation and probably reflected enhanced host defense. These data suggest that the increase in core temperature that occurs during bacterial infections is essential for optimal antimicrobial host defense.

Sephadex induces eosinophil migration to the rat and mouse peritoneal cavity: involvement of mast cells, LTB4, TNF-α, IL-8 and PAF

2002 ◽  
Vol 51 (3) ◽  
pp. 144-153 ◽  
Author(s):  
S. H. P. Oliveira ◽  
C. H. S. Costa ◽  
S. H. Ferreira ◽  
F. Q. Cunha
Keyword(s):  
Mast Cells ◽  
Peritoneal Cavity ◽  
Eosinophil Migration ◽  
Tnf Α

scholarly journals Acinetobacter baumannii LOS Regulate the Expression of Inflammatory Cytokine Genes and Proteins in Human Mast Cells

Pathogens ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 290
Author(s):  
Takane Kikuchi-Ueda ◽  
Tsuneyuki Ubagai ◽  
Go Kamoshida ◽  
Ryuichi Nakano ◽  
Akiyo Nakano ◽  
...  
Keyword(s):  
Mast Cells ◽  
Acinetobacter Baumannii ◽  
Bacterial Infections ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Bacterial Invasion ◽  
Inflammatory Genes ◽  
Human Mast Cells ◽  
Expression Of Genes ◽  
Tnf Α

Herein, we investigated the effect of bacterial lipooligosaccharides (LOS), from Acinetobacter baumannii, on the expression of pro-inflammatory genes that play an essential role in bacterial clearance. LAD2 human mast cells were stimulated with LOS derived from two strains of A. baumannii—ATCC 19606 and MDRA T14. LOS exposure induced the expression of genes for pro-inflammatory mediators, including TNF-α, IL-8, LTC4S, CCL4, and TLR4. The mRNA expression levels of a majority of the pro-inflammatory genes, except TLR4, in A. baumannii-LOS stimulated mast cells were increased. Moreover, co-culture of neutrophils with the supernatant obtained from LOS (ATCC 19606 and MDRA T14)-induced LAD2 cells increased the transmigration of neutrophils, which plays a critical role in the early protection against bacterial infections. The results of the present study suggest that LOS could be involved in the pathogenicity of A. baumannii by inducing inflammatory responses via mast cells and that IL-8 is involved in recruiting neutrophils in response to bacterial invasion.

scholarly journals TNF-alpha neutralizing antibody blocks thermal sensitivity induced by compound 48/80-provoked mast cell degranulation

F1000Research ◽  
2013 ◽  
Vol 2 ◽  
pp. 178
Author(s):  
Devavani Chatterjea ◽  
Luisa Paredes ◽  
Tijana Martinov ◽  
Evelyn Balsells ◽  
Juliann Allen ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Thermal Sensitivity ◽  
Thermal Hyperalgesia ◽  
Neutralizing Antibody ◽  
Mast Cell Degranulation ◽  
Mrna Levels ◽  
Neutrophil Influx ◽  
Environmental Stimuli ◽  
Tnf Α

Background: Neuro-inflammatory circuits in the tissue regulate the complex pathophysiology of pain. Protective nociceptive pain serves as an early warning system against noxious environmental stimuli. Tissue-resident mast cells orchestrate the increased thermal sensitivity following injection of basic secretagogue compound 48/80 in the hind paw tissues of ND4 mice. Here we investigated the effects of pre-treatment with TNF-α neutralizing antibody on compound 48/80-provoked thermal hyperalgesia.Methods: We treated ND4 Swiss male mice with intravenous anti-TNF-α antibody or vehicle 30 minutes prior to bilateral, intra-plantar compound 48/80 administration and measured changes in the timing of hind paw withdrawal observed subsequent to mice being placed on a 51oC hotplate. We also assessed changes in tissue swelling, TNF-α gene expression and protein abundance, mast cell degranulation, and neutrophil influx in the hind paw tissue.Findings: We found that TNF-α neutralization significantly blocked thermal hyperalgesia, and reduced early tissue swelling. TNF-α neutralization had no significant effect on mast cell degranulation or neutrophil influx into the tissue, however. Moreover, no changes in TNF-α protein or mRNA levels were detected within 3 hours of administration of compound 48/80.Interpretation:  The neutralizing antibodies likely target pre-formed TNF-α including that stored in the granules of tissue-resident mast cells. Pre-formed TNF-α, released upon degranulation, has immediate effects on nociceptive signaling prior to the induction of neutrophil influx. These early effects on nociceptors are abrogated by TNF-α blockade, resulting in compromised nociceptive withdrawal responses to acute, harmful environmental stimuli.

Involvement of mast cells in IL-12/23 p40 production is essential for survival from polymicrobial infections

Blood ◽  
2007 ◽  
Vol 109 (11) ◽  
pp. 4846-4855 ◽  
Author(s):  
Nobuhiro Nakano ◽  
Chiharu Nishiyama ◽  
Shunsuke Kanada ◽  
Yusuke Niwa ◽  
Naomi Shimokawa ◽  
...  
Keyword(s):  
Survival Rate ◽  
Mast Cells ◽  
Host Defense ◽  
Peritoneal Cavity ◽  
Consensus Sequence ◽  
Interleukin 12 ◽  
Mouse Bone Marrow ◽  
T Helper 1 ◽  
Important Regulator ◽  
Ifn Γ

AbstractInterleukin-12 (IL-12), a heterodimeric cytokine (p35/p40) produced mainly from macrophages and dendritic cells, is an important regulator of T-helper 1 cell responses and for host defense. We found that interferon (IFN) consensus sequence binding protein (ICSBP), which is a transcription factor essential for the expression of p40, was expressed in mouse bone marrow–derived mast cells (BMMCs). The transcription levels of p35 and p40 were increased by stimulation of BMMCs with IFN-γ/lipopolysaccharide (LPS). IL-12 was secreted from BMMCs in response to LPS but not by FcϵRI cross-linking. The p40 levels in the peritoneal cavity of mast cell–deficient W/Wv and W/Wv reconstituted with p40−/− BMMCs were significantly lower than those of WBB6F1+/+ and wild-type (WT) BMMC-reconstituted W/Wv in the acute septic peritonitis model. The survival rate of W/Wv reconstituted with p40−/− BMMCs was significantly decreased compared to those of WBB6F1+/+ and WT-BMMC–reconstituted W/Wv, which was due to reduced production of IFN-γ and subsequent impaired activation of neutrophils in the peritoneal cavity. Survival rate of p40−/− mice was also restored by adoptive transfer of WT-BMMCs. These results demonstrate that mast cells play a significant role in the production of IL-12 required for host defense. This is the first report to demonstrate that mast cells are a crucial source of functional IL-12.

scholarly journals TNF-alpha neutralizing antibody blocks thermal sensitivity induced by compound 48/80-provoked mast cell degranulation

F1000Research ◽  
2013 ◽  
Vol 2 ◽  
pp. 178 ◽  
Author(s):  
Devavani Chatterjea ◽  
Luisa Paredes ◽  
Tijana Martinov ◽  
Evelyn Balsells ◽  
Juliann Allen ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Thermal Sensitivity ◽  
Thermal Hyperalgesia ◽  
Neutralizing Antibody ◽  
Mast Cell Degranulation ◽  
Mrna Levels ◽  
Neutrophil Influx ◽  
Environmental Stimuli ◽  
Tnf Α

Background:  Neuro-inflammatory circuits in the tissue regulate the complex pathophysiology of pain.  Protective nociceptive pain serves as an early warning system against noxious environmental stimuli.  Tissue-resident mast cells orchestrate the increased thermal sensitivity following injection of basic secretagogue compound 48/80 in the hind paw tissues of ND4 mice.  Here we investigated the effects of pre-treatment with TNF-α neutralizing antibody on compound 48/80-provoked thermal hyperalgesia. Methods:  We treated ND4 Swiss male mice with intravenous anti-TNF-α antibody or vehicle 30 minutes prior to bilateral, intra-plantar compound 48/80 administration and measured changes in the timing of hind paw withdrawal observed subsequent to mice being placed on a 51oC hotplate.  We also assessed changes in tissue swelling, TNF-α gene expression and protein abundance, mast cell degranulation, and neutrophil influx in the hind paw tissue. Findings:  We found that TNF-α neutralization significantly blocked thermal hyperalgesia, and reduced early tissue swelling. TNF-α neutralization had no significant effect on mast cell degranulation or neutrophil influx into the tissue, however.  Moreover, no changes in TNF-α protein or mRNA levels were detected within 3 hours of administration of compound 48/80. Interpretation:  The neutralizing antibodies likely target pre-formed TNF-α including that stored in the granules of tissue-resident mast cells. Pre-formed TNF-α, released upon degranulation, has immediate effects on nociceptive signaling prior to the induction of neutrophil influx.  These direct effects on nociceptors are abrogated by TNF-α blockade resulting in compromised nociceptive withdrawal responses to acute, harmful environmental stimuli.

Tinospora cordifolia Aqueous Extract Alleviates Cyclophosphamide- Induced Immune Suppression, Toxicity and Systemic Candidiasis in Immunosuppressed Mice: In vivo Study in Comparison to Antifungal Drug Fluconazole

2019 ◽  
Vol 20 (12) ◽  
pp. 1055-1063 ◽  
Author(s):  
Faris Alrumaihi ◽  
Khaled S. Allemailem ◽  
Ahmad Almatroudi ◽  
Mohammed A. Alsahli ◽  
Arif Khan ◽  
...  
Keyword(s):  
Survival Rate ◽  
Aqueous Extract ◽  
Survival Data ◽  
Tinospora Cordifolia ◽  
Systemic Candidiasis ◽  
Organ Index ◽  
Tnf Α ◽  
Fungal Load ◽  
Enhanced Secretion

Objective: The present study was aimed to evaluate the effect of the aqueous extract of Tinospora cordifolia (AETC) against cyclophosphamide-induced immunosuppression and systemic Candida albicans infection in a murine model. Methods: The protective effect of AETC against cyclophosphamide-induced leukopenia was evaluated by quantitative and qualitative analysis of the leukocytes. The immune-stimulating potential of AETC on macrophages was assessed by determining the levels of secreted cytokines. To determine the direct antifungal activity, AETC or fluconazole was administered to C. albicans infected mice. The efficacy of treatment was assessed by determining the survival rate, kidney fungal burden, the organ index and liver inflammation parameters. Results: Cyclophosphamide administration resulted in substantial depletion of leukocytes, whereas AETC treatment induced the recovery of leukocytes in cyclophosphamide-injected mice. Moreover, AETC treatment of macrophages resulted in enhanced secretion of IFN-γ, TNF-α and IL-1β. C. albicans infected mice treated with AETC at the doses of 50 and 100 mg/kg exhibited 40% and 60% survival rate, whereas the mice treated with fluconazole at a dose of 50 mg/kg showed 20% survival rate. Like survival data, the fungal load was found to be the lowest in the kidney tissues of mice treated with AETC at a dose of 100 mg/kg. Interestingly, mice infected with C. albicans demonstrated improvement in the organ indices and liver functioning after AETC treatment. Conclusion: These results suggest that AETC may potentially be used to rejuvenate the weakened immune system and eliminate systemic candidiasis in mice.

scholarly journals Anti-Allergic and Anti-Inflammatory Effects of Undecane on Mast Cells and Keratinocytes

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1554
Author(s):  
Dabin Choi ◽  
Wesuk Kang ◽  
Taesun Park
Keyword(s):  
Mast Cells ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Allergic Diseases ◽  
Intracellular Camp ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Skin Conditions ◽  
Factor Α ◽  
Camp Levels

The critical roles of keratinocytes and resident mast cells in skin allergy and inflammation have been highlighted in many studies. Cyclic adenosine monophosphate (cAMP), the intracellular second messenger, has also recently emerged as a target molecule in the immune reaction underlying inflammatory skin conditions. Here, we investigated whether undecane, a naturally occurring plant compound, has anti-allergic and anti-inflammatory activities on sensitized rat basophilic leukemia (RBL-2H3) mast cells and HaCaT keratinocytes and we further explored the potential involvement of the cAMP as a molecular target for undecane. We confirmed that undecane increased intracellular cAMP levels in mast cells and keratinocytes. In sensitized mast cells, undecane inhibited degranulation and the secretion of histamine and tumor necrosis factor α (TNF-α). In addition, in sensitized keratinocytes, undecane reversed the increased levels of p38 phosphorylation, nuclear factor kappaB (NF-κB) transcriptional activity and target cytokine/chemokine genes, including thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC) and interleukin-8 (IL-8). These results suggest that undecane may be useful for the prevention or treatment of skin inflammatory disorders, such as atopic dermatitis, and other allergic diseases.

scholarly journals Human Mucosal Mast Cells Capture HIV-1 and Mediate Viraltrans-Infection of CD4+T Cells

2015 ◽  
Vol 90 (6) ◽  
pp. 2928-2937 ◽  
Author(s):  
Ai-Ping Jiang ◽  
Jin-Feng Jiang ◽  
Ji-Fu Wei ◽  
Ming-Gao Guo ◽  
Yan Qin ◽  
...  
Keyword(s):  
T Cells ◽  
Mast Cells ◽  
Cell Surface ◽  
Bacterial Infections ◽  
Mucosal Mast Cells ◽  
Mucosal Tissues ◽  
Viral Particles ◽  
Molecular Patterns ◽  
Hiv 1

ABSTRACTThe gastrointestinal mucosa is the primary site where human immunodeficiency virus type 1 (HIV-1) invades, amplifies, and becomes persistently established, and cell-to-cell transmission of HIV-1 plays a pivotal role in mucosal viral dissemination. Mast cells are widely distributed in the gastrointestinal tract and are early targets for invasive pathogens, and they have been shown to have increased density in the genital mucosa in HIV-infected women. Intestinal mast cells express numerous pathogen-associated molecular patterns (PAMPs) and have been shown to combat various viral, parasitic, and bacterial infections. However, the role of mast cells in HIV-1 infection is poorly defined. In this study, we investigated their potential contributions to HIV-1 transmission. Mast cells isolated from gut mucosal tissues were found to express a variety of HIV-1 attachment factors (HAFs), such as DC-SIGN, heparan sulfate proteoglycan (HSPG), and α4β7 integrin, which mediate capture of HIV-1 on the cell surface. Intriguingly, following coculture with CD4+T cells, mast cell surface-bound viruses were efficiently transferred to target T cells. Prior blocking with anti-HAF antibody or mannan before coculture impaired viraltrans-infection. Cell-cell conjunctions formed between mast cells and T cells, to which viral particles were recruited, and these were required for efficient cell-to-cell HIV-1 transmission. Our results reveal a potential function of gut mucosal mast cells in HIV-1 dissemination in tissues. Strategies aimed at preventing viral capture and transfer mediated by mast cells could be beneficial in combating primary HIV-1 infection.IMPORTANCEIn this study, we demonstrate the role of human mast cells isolated from mucosal tissues in mediating HIV-1trans-infection of CD4+T cells. This finding facilitates our understanding of HIV-1 mucosal infection and will benefit the development of strategies to combat primary HIV-1 dissemination.

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