Activation of Type 3 Innate Lymphoid Cells and Interleukin 22 Secretion in the Lungs During Streptococcus pneumoniae Infection

Maele, Laurye Van; Carnoy, Christophe; Cayet, Delphine; Ivanov, Stoyan; Porte, Rémi; Deruy, Emeric; Chabalgoity, José A.; Renauld, Jean‐Christophe; Eberl, Gérard; Benecke, Arndt; Trottein, François; Faveeuw, Christelle; Sirard, Jean‐Claude

doi:10.1093/infdis/jiu106

Cited by 135 publications

(161 citation statements)

References 45 publications

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“…We observed at least two populations of cells capable of producing IL-22 in the lung after challenge with MRSA. The first population comprised cells positive for IL-22, CD3, and ROR␥t, likely representing Th17 or Th22 cells (43), while the second group was negative for CD3 but positive for IL-22 and ROR␥t, possibly representing ILC3s (44).…”

Section: Discussionmentioning

confidence: 99%

Intestinal Microbiota of Mice Influences Resistance to Staphylococcus aureus Pneumonia

et al. 2015

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c Th17 immunity in the gastrointestinal tract is regulated by the intestinal microbiota composition, particularly the presence of segmented filamentous bacteria (sfb), but the role of the intestinal microbiota in pulmonary host defense is not well explored. We tested whether altering the gut microbiota by acquiring sfb influences the susceptibility to staphylococcal pneumonia via induction of type 17 immunity. Groups of C57BL/6 mice which differed in their intestinal colonization with sfb were challenged with methicillin-resistant Staphylococcus aureus in an acute lung infection model. Bacterial burdens, bronchoalveolar lavage fluid (BALF) cell counts, cell types, and cytokine levels were compared between mice from different vendors, mice from both vendors after cohousing, mice given sfb orally prior to infection, and mice with and without exogenous interleukin-22 (IL-22) or anti-IL-22 antibodies. Mice lacking sfb developed more severe S. aureus pneumonia than mice colonized with sfb, as indicated by higher bacterial burdens in the lungs, lung inflammation, and mortality. This difference was reduced when sfb-negative mice acquired sfb in their gut microbiota through cohousing with sfb-positive mice or when given sfb orally. Levels of type 17 immune effectors in the lung were higher after infection in sfb-positive mice and increased in sfb-negative mice after acquisition of sfb, as demonstrated by higher levels of IL-22 and larger numbers of IL-22؉ TCR␤ ؉ cells and neutrophils in BALF. Exogenous IL-22 protected mice from S. aureus pneumonia. The murine gut microbiota, particularly the presence of sfb, promotes pulmonary type 17 immunity and resistance to S. aureus pneumonia, and IL-22 protects against severe pulmonary staphylococcal infection.

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Section: Discussionmentioning

confidence: 99%

Intestinal Microbiota of Mice Influences Resistance to Staphylococcus aureus Pneumonia

et al. 2015

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“…IL-17A is a potent pro-inflammatory and immunostimulatory cytokine produced by T helper 17 lymphocytes, type 3 innate lymphoid cells and bovine γδ-T cells [28,29]. IL-17 is important for defence of the respiratory tract against bacterial pathogens including Staphylococcus aureus, Pseudomonas aeruginosa and Legionella pneumophila infections in mice [30][31][32].…”

Section: Discussionmentioning

confidence: 99%

Comparison of innate immune agonists for induction of tracheal antimicrobial peptide gene expression in tracheal epithelial cells of cattle

Berghuis

Abd-Elaziz

Bierworth

et al. 2014

Vet Res

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Bovine respiratory disease is a complex of bacterial and viral infections of economic and welfare importance to the beef industry. Although tracheal antimicrobial peptide (TAP) has microbicidal activity against bacterial pathogens causing bovine respiratory disease, risk factors for bovine respiratory disease including BVDV and stress (glucocorticoids) have been shown to inhibit the induced expression of this gene. Lipopolysaccharide is known to stimulate TAP gene expression, but the maximum effect is only observed after 16 h of stimulation. The present study investigated other agonists of TAP gene expression in primary cultures of bovine tracheal epithelial cells.

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“…20,50 En ratones RAG2−/− (que carecen de linfocitos T y B) infectados por vía oral con Citrobacter rodentium hubo aumento de ILC que producen IL-22 en el intestino; la eliminación de estas ILC con un anticuerpo monoclonal aceleró la muerte de dichos ratones.producción de IL-22 y la protección contra una dosis letal de esta bacteria. 59 En ratones infectados por vía oral con Salmonella enterica serovar Typhimurium, la mayor parte de las células intestinales que produjeron IFNγ fueron ILC; esta citocina se requiere para secretar el moco que protege el epitelio intestinal durante la infección y participa en la patogénesis de la enterocolitis. 60 Las ILC-3 CCR6+ (LTi-like) se encuentran en el intestino; a través de sus moléculas del MHC-II capturan, procesan y presentan antígenos de la microbiota comensal a los linfocitos T. Estas ILC-3, a diferencia de las ILC-2, carecen de moléculas coestimuladoras, por lo que causan la muerte de los linfocitos T activados con TCR específicos para antígenos de la microbiota.…”

Section: Infecciones Bacterianasunclassified

Las células linfoides innatas y su papel en la regulación de la respuesta inmune

Ruiz‐Sánchez

Cruz‐Zárate

Estrada-Garcı́a

et al. 2017

RAM

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Este artículo debe citarse como: Ruiz-Sánchez BP, Cruz-Zárate D, Estrada-García I, Wong-Baeza I. Las células linfoides innatas y su papel en la regulación de la respuesta inmune. Rev Alerg Mex. 2017;64(3):347-363 AbstractInnate lymphoid cells (ILCs) are lymphocytes lacking antigen recognition receptors and become activated in response to cytokines and through microbe-associated molecular pattern (MAMP) receptors. ILCs are found mainly in mucosal tissues and participate in the immune response against infections and in chronic inflammatory conditions. ILCs are divided in ILC-1, ILC-2 and ILC-3, and these cells have analogue functions to those of immune adaptive response lymphocytes Th1, Th2 and Th17. ILC-1 express T-bet, produce IFNγ, protect against infections with intracellular microorganisms and are related to inflammatory bowel disease immunopathology. ILC-2 express GATA3, produce IL-4, IL-5, IL-13 and amphiregulin, protect against parasitic infections and are related to allergy and obesity immunopathology. ILC-3 express ROR(γt), produce IL-17 and IL-22, protect against fungal infections and contribute to tolerance to intestinal microbiota and intestinal repair. They are related to inflammatory bowel disease and psoriasis immunopathology. In general terms, ILCs maintain homeostasis and coadjuvate in the protection against infections.

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Activation of Type 3 Innate Lymphoid Cells and Interleukin 22 Secretion in the Lungs During Streptococcus pneumoniae Infection

Cited by 135 publications

References 45 publications

Intestinal Microbiota of Mice Influences Resistance to Staphylococcus aureus Pneumonia

Intestinal Microbiota of Mice Influences Resistance to Staphylococcus aureus Pneumonia

Comparison of innate immune agonists for induction of tracheal antimicrobial peptide gene expression in tracheal epithelial cells of cattle

Las células linfoides innatas y su papel en la regulación de la respuesta inmune

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