Data on inflammatory cytokines and pathways involved in clearance of Nontypeable Haemophilus influenzae from the lungs during cigarette smoking and vitamin D deficiency

Jef Serré; Carolien Mathyssen; Tom Tanjeko Ajime; Hannelie Korf; Karen Maes; Nele Heulens; Conny Gysemans; Chantal Mathieu; Bart Vanaudenaerde; Wim Janssens; Ghislaine Gayan-Ramirez

doi:10.1016/j.dib.2018.12.048

Data on inflammatory cytokines and pathways involved in clearance of Nontypeable Haemophilus influenzae from the lungs during cigarette smoking and vitamin D deficiency

Data Brief. 2018 Dec 18:22:703-708. doi: 10.1016/j.dib.2018.12.048. eCollection 2019 Feb.

Affiliations

¹ Laboratory of Respiratory Diseases, Department of Chronic Diseases, Metabolism and Ageing (CHROMETA), KU Leuven, Leuven, Belgium.
² Laboratory of Hepatology, Department of Chronic Diseases, Metabolism and Ageing (CHROMETA), KU Leuven, Leuven, Belgium.
³ Clinical and Experimental Endocrinology, Department of Chronic Diseases, Metabolism and Ageing (CHROMETA), KU Leuven, Leuven, Belgium.

Abstract

This article contains data related to the inflammatory cytokine and investigated pathways involved in bacterial clearance reported in "Airway infection with Nontypeable Haemophilus influenzae is more rapidly eradicated in vitamin D deficient mice" (Serré et al., 2018) [1]. Vitamin D deficient or sufficient mice were oropharyngeally instilled with 10⁶ NTHi and sacrificed at 4, 8, 24 and 72 h post-infection. We measured proinflammatory cytokines (KC, TNF-α, IL-1β, IL6 and MCP-1) markers of bacterial clearance pathways (myeloid peroxidase, nitric oxide, complement C5a and immunoglobulin A) in bronchoalveolar fluid (BALF) during infection and mRNA expression levels of innate immune defense mechanism markers (mucin glycoproteins, pathogen recognitions receptor TLR2 and TLR4, antimicrobial peptides SLPI, REG3γ, lysozyme, BD-1, BD-2, BD-3 and surfactant proteins SP-A and SP-D) in lung homogenate. Finally, genomic DNA of NTHi (protein D) measured in lung homogenate was used as an indicator of NTHi invasion of alveolar macrophages or epithelial cells.