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Mucosally sourced complement factor B modulates the host response to colitis.

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Local production of Complement Factor B (CFB) in the gut mitigates colitis. Gut-derived CFB, not circulating levels, is crucial for intestinal homeostasis and mucosal defense.

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Area of Science:

  • Immunology
  • Gastroenterology
  • Molecular Biology

Background:

  • Intestinal homeostasis relies on host factors, with the complement system's role at mucosal surfaces gaining recognition.
  • The alternative complement pathway, crucial for host defense, requires Complement Factor B (CFB), but its intestinal functions are unclear.

Purpose of the Study:

  • To investigate the spatial, cellular, and functional roles of CFB in the intestine.
  • To determine if locally produced CFB impacts intestinal homeostasis and inflammatory bowel disease (IBD).

Main Methods:

  • Analysis of human colon tissue and CFB expression in IBD patients.
  • Utilized a mouse model with liver-specific CFB deficiency to isolate local gut CFB function.
  • Single-cell RNA sequencing and compartment-specific CFB deletion in mice.
  • Pharmacological CFB inhibition.

Main Results:

  • CFB is produced in the human colon and elevated in active IBD.
  • Locally synthesized CFB, not circulating CFB, protects against colitis in mice.
  • Enterocytes and fibroblasts are identified as key intestinal CFB producers.
  • Epithelial or stromal CFB deletion impairs mucosal protection.

Conclusions:

  • Complement acts as a locally regulated mucosal defense system in the intestine.
  • Gut-derived CFB is a critical factor in maintaining intestinal homeostasis.
  • CFB targeting may offer therapeutic potential for IBD.