Immune Defenses Mediated by Two ILC Subsets Are Critical for Protection against Acute Clostridium difficile Infection

Abt et al., 2015, Cell Host & Microbe 18, 27–37 July 8, 2015

Speaker: Pei-Chun Li (李姵君)                                            Time: 15:00~16:00, Oct. 28, 2015

Commentator: Jenn-Wei Chen, Ph.D (陳振暐 老師)          Place: Room 601

Abstract:

Clostridium difficile is an increasingly common clinical complication that follows antibiotic treatment-induced gut microbiota perturbation could lead infection with the enteric pathogen. Innate lymphoid cells (ILCs) are early responders to enteric pathogens. ILCs reside in the intestine and contribute to restoration of intestinal integrity following infection. [1] However, the contributions of different ILC subsets

to resolution of the acute phase of CDI remain undefined. To identify immune pathways that mediate recovery from C. difficile infection, the authors challenged C57BL/6, Rag1^-/- (lack T and B cells), and Rag2^-/- Il2rg^-/- (Ragγc^-/-) mice (lack ILCs) with C. difficile. In contrast to Rag1^-/- mice, ILC-deficient Ragγc^-/- mice rapidly succumbed to infection. To identify the protection against infection restored by transferring ILCs into Ragγc^-/- mice. Ragγc^-/- ILC recipient mice had reduced morbidity and mortality following infection compared to Ragγc^-/- mice not receiving ILCs, demonstrating the capacity of ILCs to promote recovery from acute CDI. This report identifies the critical role of ILC1s in host defense against C. difficile and suggests the potential for a cooperative role of ILC1s and ILC3s in limiting pathology following pathogen-induced damage to the epithelial barrier.

References:

1.     Artis, D., and Spits, H. (2015). The biology of innate lymphoid cells. Nature 517, 293–301.