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Background

Inflammation contributes to heart failure (HF) development, the progression from left ventricular failure to pulmonary remodeling, and the consequent right ventricular hypertrophy and failure. NK1.1 plays a critical role in Natural killer (NK) and NK T (NKT) cells, but the role of NK1.1 in HF development and progression is unknown.

Methods

We studied the effects of NK1.1 inhibition on transverse aortic constriction (TAC)-induced cardiopulmonary inflammation, HF development, and HF progression in immunocompetent male mice of C57BL/6J background.

Results

We found that NK1.1+ cell-derived interferon gamma+ (IFN-γ+) was significantly increased in pulmonary tissues after HF. In addition, anti-NK1.1 antibodies simultaneously abolished both NK1.1+ cells, including the NK1.1+NK and NK1.1+NKT cells in peripheral blood, spleen, and lung tissues, but had no effect on cardiopulmonary structure and function under control conditions. However, systemic inhibition of NK1.1 signaling by anti-NK1.1 antibodies significantly rescued mice from TAC-induced left ventricular inflammation, fibrosis, and failure. Inhibition of NK1.1 signaling also significantly attenuated TAC-induced pulmonary leukocyte infiltration, fibrosis, vessel remodeling, and consequent right ventricular hypertrophy. Moreover, inhibition of NK1.1 signaling significantly reduced TAC-induced pulmonary macrophage and dendritic cell infiltration and activation.

Conclusions

Our data suggest that inhibition of NK1.1 signaling is effective in attenuating systolic overload-induced cardiac fibrosis, dysfunction, and consequent pulmonary remodeling in immunocompetent mice through modulating the cardiopulmonary inflammatory response."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.org/dc/terms/identifier"doi:10.3389/fimmu.2023.1215855"xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/author"He X."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/author"Pan L."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/author"Zeng H."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/author"Xu R."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/author"Chen J.X."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/author"Hall M.E."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/author"Bhattarai U."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/name"Front Immunol"xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/pages"1215855"xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/title"Inhibition of NK1.1 signaling attenuates pressure overload-induced heart failure, and consequent pulmonary inflammation and remodeling."xsd:string
http://purl.uniprot.org/citations/37554327http://purl.uniprot.org/core/volume"14"xsd:string
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