CCL28 modulates neutrophil responses during infection with mucosal pathogens.

Autor:	Walker GT; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States., Perez-Lopez A; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States.; Department of Microbiology and Molecular Genetics, University of California Irvine, Irvine, United States.; Biomedicine Research Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, Mexico., Silva S; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States., Lee MH; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States., Bjånes E; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States., Dillon N; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States.; Department of Biological Sciences, University of Texas at Dallas, Richardson, United States., Brandt SL; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States., Gerner RR; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States.; School of Life Sciences, ZIEL - Institute for Food and Health, Freising-Weihenstephan, Technical University of Munich, Munich, Germany., Melchior K; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States.; School of Pharmaceutical Sciences, São Paulo State University (UNESP), Araraquara, São Paulo, Brazil., Norton GJ; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States., Argueta FA; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States., Dela Pena F; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States., Park L; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States., Sosa-Hernandez VA; Red de Apoyo a la Investigación, Universidad Nacional Autónoma de México and Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México City, Mexico.; Departamento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Mexico City, Mexico., Cervantes-Diaz R; Red de Apoyo a la Investigación, Universidad Nacional Autónoma de México and Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México City, Mexico.; Departamento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Mexico City, Mexico., Romero-Ramirez S; Red de Apoyo a la Investigación, Universidad Nacional Autónoma de México and Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México City, Mexico.; Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico., Cartelle Gestal M; Department of Microbiology and Immunology, Louisiana State University Health Sciences Center at Shreveport, Shreveport, United States., Maravillas-Montero JL; Red de Apoyo a la Investigación, Universidad Nacional Autónoma de México and Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México City, Mexico., Nuccio SP; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States.; Department of Microbiology and Molecular Genetics, University of California Irvine, Irvine, United States., Nizet V; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States.; Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, La Jolla, United States.; Center for Microbiome Innovation, University of California San Diego, La Jolla, United States., Raffatellu M; Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, La Jolla, United States.; Department of Microbiology and Molecular Genetics, University of California Irvine, Irvine, United States.; Center for Microbiome Innovation, University of California San Diego, La Jolla, United States.; Chiba University-UC San Diego Center for Mucosal Immunology, Allergy, and Vaccines (CU-UCSDcMAV), La Jolla, United States.
Jazyk:	angličtina
Zdroj:	ELife [Elife] 2024 Aug 28; Vol. 13. Date of Electronic Publication: 2024 Aug 28.
DOI:	10.7554/eLife.78206
Abstrakt:	The chemokine CCL28 is highly expressed in mucosal tissues, but its role during infection is not well understood. Here, we show that CCL28 promotes neutrophil accumulation in the gut of mice infected with Salmonella and in the lung of mice infected with Acinetobacter . Neutrophils isolated from the infected mucosa expressed the CCL28 receptors CCR3 and, to a lesser extent, CCR10, on their surface. The functional consequences of CCL28 deficiency varied between the two infections: Ccl28 -/- mice were highly susceptible to Salmonella gut infection but highly resistant to otherwise lethal Acinetobacter lung infection. In vitro, unstimulated neutrophils harbored pre-formed intracellular CCR3 that was rapidly mobilized to the cell surface following phagocytosis or inflammatory stimuli. Moreover, CCL28 stimulation enhanced neutrophil antimicrobial activity, production of reactive oxygen species, and formation of extracellular traps, all processes largely dependent on CCR3. Consistent with the different outcomes in the two infection models, neutrophil stimulation with CCL28 boosted the killing of Salmonella but not Acinetobacter . CCL28 thus plays a critical role in the immune response to mucosal pathogens by increasing neutrophil accumulation and activation, which can enhance pathogen clearance but also exacerbate disease depending on the mucosal site and the infectious agent. Competing Interests: GW, AP, SS, ML, EB, ND, SB, RG, KM, GN, FA, FD, LP, VS, RC, SR, MC, JM, SN, VN, MR No competing interests declared (© 2024, Walker, Perez-Lopez et al.)
Databáze:	MEDLINE
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