scholarly journals Evaluation of Bifidobacteria and Lactobacillus Probiotics as Alternative Therapy for Salmonella typhimurium Infection in Broiler Chickens

Animals ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 1023 ◽  
Author(s):  
Hanem El-Sharkawy ◽  
Amin Tahoun ◽  
Amira M. Rizk ◽  
Tohru Suzuki ◽  
Walid Elmonir ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Epithelial Cells ◽  
Broiler Chickens ◽  
Competitive Exclusion ◽  
Enteric Bacteria ◽  
Host Cells ◽  
Economic Losses ◽  
Tnf Α ◽  
Probiotic Strains ◽  
Ifn Γ

Chicken Salmonella enterica serovars are enteric bacteria associated with massive public health risks and economic losses. There is a widespread antimicrobial resistance among S. enterica serotypes, and innovative solutions to antibiotic resistance are needed. We aimed to use probiotics to reduce antibiotic resistance and identify the major probiotic players that modify the early interactions between S. enterica and host cells. One-day-old cobb broiler chicks were challenged with S. typhimurium after oral inoculation with different probiotic strains for 3 days. The adherence of different probiotic strains to Caco-2 intestinal epithelial cells was studied in vitro. Lactobacillus (Lacticaseibacillus) casei ATTC334 and Bifidobacterium breve JCM1192 strains attached to Caco-2 cells stronger than B. infantis BL2416. L. casei ATTC334 and B. breve JCM1192 reduced S. typhimurium recovery from the cecal tonsils by competitive exclusion mechanism. Although B. infantis BL2416 bound poorly to Caco-2 epithelial cells, it reduced S. typhimurium recovery and increased IFN-γ and TNF-α production. L. casei ATTC334, B. breve JCM1192 and B. infantis BL2416 improved body weight gain and the food conversion rate in S. typhimurium-infected broilers. B. longum Ncc2785 neither attached to epithelial cells nor induced IFN-γ and TNF-α release and consequently did not prevent S. typhimurium colonization in broiler chickens. In conclusion, probiotics prevented the intestinal colonization of S. typhimurium in infected chickens by competitive exclusion or cytokine production mechanisms.

Evaluation of the Role of Staphylococci in the Pathomechanism of Conjunctivitis

2021 ◽  
Author(s):  
Ewa Jasińska ◽  
Agnieszka Bogut ◽  
Agnieszka Magryś ◽  
Alina Olender
Keyword(s):  
Antibiotic Resistance ◽  
Epithelial Cells ◽  
Biofilm Formation ◽  
Methicillin Resistance ◽  
Microtiter Plate ◽  
Host Cells ◽  
Diffusion Method ◽  
Microtiter Plate Assay ◽  
Low Prevalence

Abstract Purpose: Determination of the association between ica genes and phenotypic biofilm formation in staphylococcal isolates involved in conjunctivitis, their antibiotic resistance as well as detection of selected virulence characteristics: adhesion to epithelial cells and in vitro cytotoxicity.Methods: The study included 26 Staphylococcus aureus (SA) and 26 Staphylococcus epidermidis (SE) isolates. The presence of icaAD genes and ica operon was determined by the PCR assay. Phenotypic biofilm formation was verified using the microtiter plate assay. Antibiotic resistance was performed using the disc diffusion method. Staphylococcal ability to attach to host cells was assessed by flow cytometry. Cytotoxicity on epithelial cells was evaluated by LDH assay.Results: The ica genes were detected in 26.9% of SE and in 42.3% of SA isolates. Only 15.3% of isolates (SE) were positive for both the icaAD and the ica operon. Phenotypically, 19.2% of SE isolates were strong biofilm producers, among which three were both icaAD- and ica operon-positive. 26.9% of SA isolates were strong biofilm producers. Methicillin resistance (MR) was detected in 34.6% of SE and 26.9% of SA isolates. 75% of MR isolates were multidrug resistant. SA isolates adhered to host cells more extensively than SE. SA isolates released higher level of LDH than SE.Conclusions: Adherence abilities were commonly observed in staphylococci associated with conjunctivitis. However, low prevalence of isolates positive for a complete and functional ica locus and low prevalence of strong biofilm producers was detected. SA adhered to a greater extent to eukaryotic cells than SE and were more cytotoxic.

Proinflammatory cytokines TNF-α and IFN-γ alter laminin expression under an apoptosis-independent mechanism in human intestinal epithelial cells

2004 ◽  
Vol 287 (3) ◽  
pp. G592-G598 ◽  
Author(s):  
Caroline Francoeur ◽  
Fabrice Escaffit ◽  
Pierre H. Vachon ◽  
Jean-François Beaulieu
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Proinflammatory Cytokines ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Laminin 5 ◽  
Cell Functions ◽  
Tnf Α ◽  
Independent Mechanism ◽  
Ifn Γ

Laminins are basement membrane molecules that mediate cell functions such as adhesion, proliferation, migration, and differentiation. In the normal small intestine, laminin-5 and -10 are mainly expressed at the base of villus cells. However, in Crohn's disease (CD), a major redistribution of these laminins to the crypt region of the inflamed ileal mucosa has been observed, suggesting a possible relationship between laminin expression and cytokine and/or growth factor production, which is also altered in CD. The aim of this study was to test the hypothesis that proinflammatory cytokines can modulate laminin expression by intestinal epithelial cells. The effect of TNF-α, IFN-γ, IL-1β, IL-6, and transforming growth factor (TGF)-β was analyzed on the expression of laminins in the normal human intestinal epithelial crypt (HIEC) cell line. When treated with a single cytokine, HIEC cells secreted small amounts of laminin-5 and -10. Only TNF-α and TGF-β induced a slight increase in the secretion of these laminins. However, in combination, TNF-α and IFN-γ synergistically stimulated the secretion of both laminin-5 and -10 in HIEC cells. Transcript analyses suggested that the upregulation of the two laminins might depend on distinct mechanisms. Interestingly, the TNF-α and IFN-γ combination was also found to significantly promote apoptosis. However, the effect of cytokines on the secretion of laminins was maintained even after completely blocking apoptosis by inhibiting caspase activities. These results demonstrate that laminin production is specifically modulated by the proinflammatory cytokines TNF-α and IFN-γ in intestinal epithelial cells under an apoptosis-independent mechanism.

scholarly journals The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract

2013 ◽  
Vol 18 (4) ◽  
Author(s):  
Magdalena Paplińska-Goryca ◽  
Patrycja Nejman-Gryz ◽  
Ryszarda Chazan ◽  
Hanna Grubek-Jaworska
Keyword(s):  
Epithelial Cells ◽  
Respiratory Tract ◽  
Airway Epithelial Cells ◽  
Small Airway ◽  
Primary Cells ◽  
Human Epithelial Cells ◽  
Tnf Α ◽  
Normal Human ◽  
Ifn Γ ◽  
Pre Treatment

AbstractAirway epithelium acts as multifunctional site of response in the respiratory tract. Epithelial activity plays an important part in the pathophysiology of obstructive lung disease. In this study, we compare normal human epithelial cells from various levels of the respiratory tract in terms of their reactivity to pro-allergic and pro-inflammatory stimulation. Normal human nasal, bronchial and small airway epithelial cells were stimulated with IL-4 and IL-13. The expressions of the eotaxins IL-6 and CXCL8 were evaluated at the mRNA and protein levels. The effects of pre-treatment with IFN-γ on the cell reactivity were measured, and the responses to TNF-α, LPS and IFN-γ were evaluated. All of the studied primary cells expressed CCL26, IL-6 and IL-8 after IL-4 or IL-13 stimulation. IFN-γ pre-treatment resulted in decreased CCL26 and increased IL-6 expression in the nasal and small airway cells, but this effect was not observed in the bronchial cells. IL-6 and CXCL8 were produced in varying degrees by all of the epithelial primary cells in cultures stimulated with TNF-α, LPS or IFN-γ. We showed that epithelial cells from the various levels of the respiratory tract act in a united way, responding in a similar manner to stimulation with IL-4 and IL-13, showing similar reactivity to TNF-α and LPS, and giving an almost unified response to IFN-γ pre-stimulation.

TNF-α and IFN-γ regulate the expression of the NOD2 (CARD15) gene in human intestinal epithelial cells

2003 ◽  
Vol 124 (4) ◽  
pp. 1001-1009 ◽  
Author(s):  
Philip Rosenstiel ◽  
Massimo Fantini ◽  
Karen Bräutigam ◽  
Tanja Kühbacher ◽  
Georg H. Waetzig ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Card15 Gene

TNF-α and IFN-γ regulate the expression of the NOD2 (CARD15) gene in human intestinal epithelial cells

2003 ◽  
Vol 124 (4) ◽  
pp. A111 ◽  
Author(s):  
Philip Rosenstiel ◽  
Massimo Fantini ◽  
Karen Braeutigam ◽  
Georg Waetzig ◽  
Tanja Kuehbacher ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Card15 Gene

scholarly journals Peptide vaccines designed with the aid of immunoinformatic against Caseous Lymphadenitis promotes humoral and cellular response induction in mice

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0256864
Author(s):  
Daniela Droppa-Almeida ◽  
Glenda Amaral da Silva ◽  
Lívia Maria do Amorim Costa Gaspar ◽  
Beatriz Benny Sungaila Pereyra ◽  
Roberto José Meyer Nascimento ◽  
...  
Keyword(s):  
Cellular Response ◽  
Small Ruminants ◽  
Study Groups ◽  
Economic Losses ◽  
Caseous Lymphadenitis ◽  
Peptide Vaccines ◽  
Tnf Α ◽  
Ifn Γ ◽  
Humoral And Cellular Response ◽  
Immunodominant Epitopes

Caseous Lymphadenitis (CLA) is a chronic disease that affects also small ruminants. CLA is caused by Corynebacterium pseudotuberculosis and is responsible for high economic losses due to the formation of superficial and visceral granulomas, the latter is considered as asymptomatic CLA causing high levels of dissemination. Several vaccination strategies, in which the use of synthetic peptides stands out. Thus, this work aimed to evaluate the protective potential of peptide vaccines designed to determine the immunodominant epitopes of CP40 against CLA in mice. The animals were divided into eight groups separated in controls (G1—PBS, G2—Saponin and G9—rCP40) and experimental (G3—pep1, G4- pep2, G5-pep3, G6-pep4, G7-pep5 and G8-pep6), these were vaccinated on days 0 and 15 by a subcutaneous route. 60 days after the first immunization, all animals were challenged with C. pseudotuberculosis. On days 0, 15, 60, and 120 after the first immunization, blood samples were taken to measure immunoglobulins. On the same day of the challenge, the splenocytes were isolated and assayed for the production of IL-2, IL-4, IL-6, IFN-γ, TNF-α, IL-17, and IL-10. After vaccinations, the animals were challenged and all of them were affected by the disease which led to their death. The G6 and G8 groups provided 10% protection and the G7 provided 20%. The G3 and G4 groups provided 30% and 40% protection respectively. The peptides showed the production of Total IgG antibodies and cytokines (IL-2, IL-4, IL-6, IFN-γ, and TNF-α), indicating a possible activation of the Th1 type response. However, groups G3, G5, G6, and G8 showed production of IL-17. None of the study groups showed IL-10 production. The immunogenicity of the peptides was not enough to protect these animals and it is believed that the use of adjuvants based on PAMPs may improve the immune response offered by these peptides.

Silica-induced chemokine expression in alveolar type II cells is mediated by TNF-α

1998 ◽  
Vol 275 (6) ◽  
pp. L1110-L1119 ◽  
Author(s):  
Edward G. Barrett ◽  
Carl Johnston ◽  
Günter Oberdörster ◽  
Jacob N. Finkelstein
Keyword(s):  
Epithelial Cells ◽  
Cell Line ◽  
Rnase Protection Assay ◽  
Alveolar Type ◽  
Mrna Levels ◽  
Type Ii ◽  
Rnase Protection ◽  
Tnf Α ◽  
Type Ii Cell ◽  
Ifn Γ

Recent evidence has suggested that epithelial cells may contribute to the inflammatory response in the lung after exposure to crystalline silica through the production of and response to specific growth factors, chemokines, and cytokines. However, the exact cellular and molecular responses of epithelial cells to silica exposure remains unclear. Using a murine alveolar type II cell line [murine lung epithelial (MLE)-15 cell line], we measured the early changes in various cytokine and chemokine mRNA species after exposure of the cells to 4–35 μg/cm2 of silica (cristobalite), interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and lipopolysaccharide (LPS) alone or in combination. Total mRNA was isolated and assayed with an RNase protection assay after 6 and 24 h of exposure. Cristobalite exposure alone led to an increase in monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-2, and regulated on activation normal T cells expressed and secreted (RANTES) mRNAs. Treatment with IFN-γ alone increased MCP-1 mRNA levels. Treatment with TNF-α or LPS alone led to an increase in MCP-1 and MIP-2 mRNA. The combination of cristobalite plus TNF-α led to an additive increase in MCP-1 and MIP-2, whereas cristobalite plus IFN-γ or LPS had a synergistic effect. We also found with a TNF-α-neutralizing antibody that TNF-α plays a major role in mediating the type II cell chemokine response to cristobalite exposure. The results indicate that the cristobalite-induced chemokine response in the lung epithelium is mediated in part by TNF-α and can be enhanced by macrophage- and lymphocyte-derived inflammatory mediators in an additive and synergistic fashion.

scholarly journals Effector CD8+T Cells Are Generated in Response to an Immunodominant Epitope in Type III Effector YopE during Primary Yersinia pseudotuberculosis Infection

2014 ◽  
Vol 82 (7) ◽  
pp. 3033-3044 ◽  
Author(s):  
Yue Zhang ◽  
Patricio Mena ◽  
Galina Romanov ◽  
James B. Bliska
Keyword(s):  
T Cells ◽  
Primary Infection ◽  
Yersinia Pseudotuberculosis ◽  
Intracellular Cytokine Staining ◽  
Host Cells ◽  
Membrane Localization ◽  
Content Type ◽  
Terminal Domain ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACTYopE is a virulence factor that is secreted into host cells infected byYersiniaspecies. The YopE C-terminal domain has GTPase-activating protein (GAP) activity. The YopE N-terminal domain contains an epitope that is an immunodominant CD8+T cell antigen during primary infection of C57BL/6 mice withYersinia pseudotuberculosis. The characteristics of the CD8+T cells generated in response to the epitope, which comprises YopE amino acid residues 69 to 77 (YopE69–77), and the features of YopE that are important for antigenicity during primary infection, are unknown. Following intravenous infection of naïve C57BL/6 mice with ayopEGAP mutant (the R144A mutant), flow cytometry analysis of splenocytes by tetramer and intracellular cytokine staining over a time course showed that YopE69–77-specific CD8+T cells producing gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α) were generated by day 7, with a peak at day 14. In addition, ∼80% of YopE69–77-specific CD8+T cells were positive for KLRG1, a memory phenotype marker, at day 21. To determine if residues that regulate YopE activity by ubiquitination or membrane localization affect the antigenicity of YopE69–77, mice were infected with ayopEubiquitination or membrane localization mutant (the R62K or L55N I59N L63N mutant, respectively). These mutants elicited YopE69–77-specific CD8+T cells producing IFN-γ and TNF-α with kinetics and magnitudes similar to those of the parental R144A strain, indicating that primary infection primes effector CD8+T cells independently of the ubiquitination or membrane localization of YopE. Additionally, at day 7, there was an unexpected positive correlation between the numbers of YopE69–77-specific CD8+T cells and CD11b+cells, but not between the numbers of YopE69–77-specific CD8+T cells and bacterial cells, in spleens, suggesting that the innate immune response contributes to the immunodominance of YopE69–77.

Human intestinal intraepithelial lymphocytes and epithelial cells coinduce interleukin-8 production through the CD2-CD58 interaction

2009 ◽  
Vol 296 (3) ◽  
pp. G671-G677 ◽  
Author(s):  
Ellen C. Ebert ◽  
Asit Panja ◽  
Rajalakshmi Praveen
Keyword(s):  
Epithelial Cells ◽  
Cell Types ◽  
Interferon Γ ◽  
Intraepithelial Lymphocytes ◽  
Cell Contact ◽  
Tnf Α ◽  
Active Transcription ◽  
Ifn Γ ◽  
Factor Α ◽  
Ht 29

Human intestinal CD3+TCRαβ+CD8+ intraepithelial lymphocytes (IELs) are intimately associated with epithelial cells (ECs) through binding of CD103 to E-cadherin. How these two cell types functionally interact is largely unknown. IEL-EC cross talk was determined using HT-29 cells as the model EC and IL-8 as the readout. IL-8 was derived from both cell types and synergistically increased when the cells were combined. This synergistic effect required active transcription by both IELs and HT-29 cells. Cell contact was required as shown by the loss of the synergistic increase in IL-8 when the two cell types were separated by Transwells. Specifically, IL-8 release required the binding of CD2 on the IELs to CD58 on the HT-29 cells. The association of the CD3/TCR complex with major histocompatibility antigen class I antigens was not involved. Antibody neutralization of tumor necrosis factor-α (TNF-α), but not interferon-γ (IFN-γ), resulted in increased IL-8 production by the coculture. Although both TNF-α and IFN-γ increased IL-8 synthesis and CD58 expression by the HT-29 cells, only IFN-γ reduced IL-8 production by IELs. IL-8 production by either cell type involved phosphorylation of p38 and JNK. In summary, the synergistic synthesis of IL-8 occurs when IELs are stimulated through the CD2 pathway by CD58 on HT-29 cells, resulting in TNF-α release that, in turn, augments IL-8 synthesis and CD58 expression by the HT-29 cells.

Self-antigen expression in thymic epithelial cells in Ifn-γ or Tnf-α deficiency

Cytokine ◽  
2013 ◽  
Vol 62 (3) ◽  
pp. 433-438
Author(s):  
Dina Levi ◽  
Constantin Polychronakos
Keyword(s):  
Epithelial Cells ◽  
Antigen Expression ◽  
Thymic Epithelial Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Self Antigen
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