Adoptive Transfer of Group 3-Like Innate Lymphoid Cells Restores Mouse Colon Resistance to Colonization of a Gamma Interferon-Susceptible Chlamydia muridarum Mutant.

The obligate intracellular bacterium can colonize the mouse colon for a long period, but a gamma interferon (IFN-γ)-susceptible mutant clone fails to do so. Nevertheless, the mutant's colonization is rescued in mice deficient in interleukin-7 receptor (IL-7R) (lacking both lymphocytes and innate lymphoid cells [ILCs]) or IFN-γ but not in mice lacking recombination-activated gene 1 (Rag1 mice) (lacking adaptive immunity lymphocytes), indicating a critical role of ILC-derived IFN-γ in regulating chlamydial colonization. In the current study, we have used an adoptive transfer approach for further characterizing the responsible ILCs.

Evasion of Innate Lymphoid Cell-Regulated Gamma Interferon Responses by Chlamydia muridarum To Achieve Long-Lasting Colonization in Mouse Colon.

Revealing the mechanisms by which bacteria establish long-lasting colonization in the gastrointestinal tract is an area of intensive investigation. The obligate intracellular bacterium is known to colonize mouse colon for long periods. A colonization-deficient mutant strain of this intracellular bacterium is able to regain long-lasting colonization in gamma interferon (IFN-γ) knockout mice following intracolon inoculation.

Distinct Roles of Chromosome- versus Plasmid-Encoded Genital Tract Virulence Factors in Promoting Chlamydia muridarum Colonization in the Gastrointestinal Tract.

The genital pathogen is known to colonize the gastrointestinal tract. Orally delivered can reach the colon and maintain a long-lasting colonization there. However, with mutations in chromosomal genes and (designated a chromosomal mutant) or deficient in plasmid-encoded pGP3 (designated a plasmid mutant) is unable to do so.

Antigen-Specific CD4 T Cell-Derived Gamma Interferon Is Both Necessary and Sufficient for Clearing from the Small Intestine but Not the Large Intestine.

The genital tract pathogen is frequently detected in the gastrointestinal tract, but the host immunity that regulates chlamydial colonization in the gut remains unclear. In a -C57 mouse model, chlamydial organisms are cleared from the genital tract in ∼4 weeks, but the genital organisms can spread to the gastrointestinal tract. We found that the gastrointestinal chlamydial organisms were cleared from the small intestine by day 28, paralleling their infection course in the genital tract, but persisted in the large intestine for long periods.