T Cells Help To Amplify Inflammatory Responses Induced by<i>Salmonella enterica</i>Serotype Typhimurium in the Intestinal Mucosa

Godinez, Ivan; Haneda, Takeshi; Raffatellu, Manuela; George, Michael; Paixão, Tatiane Alves; Rolán, Hortensia G.; Santos, Renato L.; Dandekar, Satya; Tsolis, Renée M.; Bäumler, Andreas J.

doi:10.1128/iai.01691-07

Cited by 137 publications

(137 citation statements)

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“…2 and reference 19 ), and by crypt and villus EC, IL-17A-producing cells may participate in immunosurveillance in an enteric environment. Interleukin-17A elicits the expression of antimicrobial factors, such as BD3, lopocalin-2 and S100A8/9 proteins in collaboration with IL-22, 7,20 suggesting that IL-17A-producing cells in LP enable the suppression of the invasion of pathogens through the induction of antimicrobial factors. Beta-defensin-3 is a candidate of the IL-17A-dependent immediate early protective effector because it is constitutively expressed at the epithelial surface of intestinal mucosa in an IL-17A-dependent manner, and S. typhimurium was reported to be resistant to lipocalin-2.…”

Section: Discussionmentioning

confidence: 99%

“…6 Especially, interferon-c (IFN-c), interleukin-17A (IL-17A) and IL-22 have been reported to increase during the early period of enteric S. typhimurium infection. 7 The T helper type 1 (Th1) immune response is well known to be essential for the control of Salmonella infection in mice and humans; 8,9 indeed, IFN-c-deficient mice are susceptible to S. typhimurium infection. 10 The other host strategy for controlling the colonization and dissemination of the pathogens is to limit their thriving by producing antimicrobial factors to support the host defence mechanism before induction of Th1-acquired immunity.…”

Section: Discussionmentioning

confidence: 99%

“…[8][9][10] Recently, the role of IL-17A in protective immunity against Salmonella and other intracellular bacteria has been reported. 7,14,25,26 Therefore, to clarify the mechanism of the early protective response against intestinal S. typhimurium infection, we examined the kinetics of IFN-c-producing and IL-17A-producing T cells in the GALT during S. typhimurium infection. The total cell number of LPL and MLN increased following S. typhimurium infection, whereas numbers of IEL and PP did not (Fig.…”

Section: Constitutive Expression Of Il-17a and Induced Expression Of mentioning

confidence: 99%

“…7,14 Interleukin-17A was originally reported as an inflammatory cytokine, which is produced by CD4 + T-cell receptor (TCR) -ab T cells. It induces the differentiation and chemotaxis of neutrophils 15 and contributes to the elimination of pathogens or induces inflammatory autoimmune diseases.…”

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confidence: 99%

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Interleukin‐17A is required to suppress invasion of Salmonella enterica serovar Typhimurium to enteric mucosa

et al. 2010

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Summary Salmonella enterica serovar Typhimurium (S. typhimurium) causes a localized enteric infection and its elimination is dependent on a T helper type 1 immune response. However, the mechanism of the protective immune response against the pathogen in gut‐associated lymphoid tissue (GALT) at an early stage of the infection is not yet clarified. Here, we show that interleukin‐17A (IL‐17A) was constitutively expressed in GALT; it was also detected on crypt and epithelial cells of the small intestine. Neutralization of the IL‐17A in the intestinal lumen exacerbated epithelial damage induced by intestinal S. typhimurium infection at an early stage of the infection. The result suggests that IL‐17A has a pivotal role in the immediate early stage of protection against bacterial infection at the intestinal mucosa. As IL‐17A neutralization also suppressed the constitutive localization of β‐defensin 3 (BD3), an IL‐17A‐induced antimicrobial peptide, at the apical site of the intestinal mucosa, it is estimated that IL‐17A constitutively induces the expression of the antimicrobial peptide to kill invading pathogens at the epithelial surface immediately after the infection. In contrast, interferon‐γ is induced around 3 days after S. typhimurium infection, and its expression level increases thereafter. Taken together, the findings lead to the hypothesis that IL‐17A participates in the immediate early stage of protection against S. typhimurium intestinal infection whereas interferon‐γ is important at a later stage of the infection.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Constitutive Expression Of Il-17a and Induced Expression Of mentioning

confidence: 99%

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Interleukin‐17A is required to suppress invasion of Salmonella enterica serovar Typhimurium to enteric mucosa

et al. 2010

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“…Typhoid fever is characterized by a persistent high fever, headache, profuse sweating, nausea, vomiting, abdominal pain, ileal perforation, diarrhea, liver abscess, gastroenteritis, bradycardia, hepatomegaly and splenomegaly (Godinez et al 2008). S. Typhi is transmitted through contaminated food and water; following ingestion, the bacteria spread from the intestine via blood to the intestinal lymph nodes, liver, and spleen where they multiply.…”

Section: Introductionmentioning

confidence: 99%

Protection against experimental salmonellosis by recombinant 49 kDa OMP of Salmonella enterica serovar Typhi: biochemical aspects

Kaur

Jain

2013

Biologia

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Typhoid fever is systemic illness caused by Salmonella enterica serovar Typhi (S. Typhi) in humans. Increasing multidrug resistant strains of S. Typhi and limited effect of available vaccines has necessitated exploring of new immunogens for protection against it. Earlier studies have shown that a crude preparation of outer membrane proteins (OMPs) of S. Typhi evokes strong immune response and induces a protective immunity against infection caused by diverse Gram-negative bacteria. In the present study we have evaluated the protective effect of a purified recombinant 49 kDa (r49kDa) OMP of S. Typhi alone or along with alum or complete Freund's adjuvant, against a challenge by S. Typhi (0.4 × 50% lethal dose) by biochemical estimation of serum enzymes and oxidative stress enzymes in Swiss albino mice. There was a decrease in activity of alanine aminotransferase by 14.28%, 38.09%, 23.80%; aspartate aminotransferase by 6.25%, 25%, 16.25%; lipid peroxidation by 4.34%, 18.84%, 11.59%; and catalase by 8%, 14%, 10%, respectively, whereas increase in activity of reduced glutathione by 33.33%, 61.11%, 44.44%; glutathione peroxidase by 7%, 16%, 10%; and glutathione reductase by 8%, 20%, 12%, respectively, as compared to control animals challenged with bacteria without pre-immunization. The results indicated that immunization of mice with r49kDa OMP alone or in combination with adjuvants protected and normalized the liver. It reduces the development of oxidative stress in mice against Salmonella infection and the risk of getting typhoid. These results represent an additional supplement to our earlier reported data on protective immunity evoked by this protein.

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Mechanisms of Dysbiosis in the Inflamed Gut

Winter¹

2016

Host – Pathogen Interaction

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T Cells Help To Amplify Inflammatory Responses Induced bySalmonella entericaSerotype Typhimurium in the Intestinal Mucosa

Cited by 137 publications

References 40 publications

Interleukin‐17A is required to suppress invasion of Salmonella enterica serovar Typhimurium to enteric mucosa

Interleukin‐17A is required to suppress invasion of Salmonella enterica serovar Typhimurium to enteric mucosa

Protection against experimental salmonellosis by recombinant 49 kDa OMP of Salmonella enterica serovar Typhi: biochemical aspects

Mechanisms of Dysbiosis in the Inflamed Gut

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