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

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.

Airway infection with Nontypeable Haemophilus influenzae is more rapidly eradicated in vitamin D deficient mice

“…4C). Inflammatory mediator levels were similar between vitamin D deficient and sufficient mice during the first 24 h post-infection (Table 1 in [31]). However, a significant decrease in IL6 (Fig.…”

“…Chromosomal DNA concentration of NTHi in lung homogenate decreased overtime and could no longer be detected 72 h post-infection with no significant differences between vitamin D deficient and sufficient mice (Fig. 2 in [31]). Total number of macrophages gradually increased at each time point but did not significantly differ between vitamin D deficient and sufficient mice (Fig.…”

“…mRNA expression levels of PRR's, AMP's and SP's in the lung were similarly enhanced in both groups during the course of infection and post-infection (Table 3 in [31]), while mucin glycoproteins, MUC5B and MUC5AC, mRNA were solely enhanced late post-infection particularly in vitamin D deficient mice (Table 3 in [31]). There was also a trend for TLR4 mRNA to be higher in vitamin D deficient mice (Table 3 in [31]). By contrast, the mRNA expression of CRAMP in the lung was significantly upregulated in vitamin D deficient mice during the whole infection period (p = 0.026) (Fig.…”

“…We examined the expression of main described pattern recognition receptors (PRR), antimicrobial peptides (AMP) and surfactant proteins (SP): toll-like receptor (TLR) 2, lysozyme, secreted leukocyte protease inhibitor (SLPI), β-defensin 1, 2, 3 and cathelicidin related antimicrobial peptide (CRAMP), regenerating islet-derived protein 3-gamma (REG3γ), SP-A and D. In addition, we looked for a misbalance of proteases and anti-proteases: MMP9, MMP12 and tissue inhibitor of MMP (TIMP) 1. Primer sequences are shown in Table 2 in [31].…”

Clinical effect of vitamin�D supplementation on patients with pulmonary tuberculosis and its influence on the expression of immune cells and inflammatory factors

“…Both treatment methods improved the content of surfactant protein after treatment, and vitamin D auxiliary treatment effectively reduced the levels of SP-A and SP-D. Animal experimental research has revealed that SP-D levels in mice with sufficient vitamin D before and after infection are lower than those in mice with insufficient vitamin D ( 35 ). Since the serum level of the patients was tested in this study at 3 months after treatment, we did not know the long-term changing trend of surfactant protein, thus the effect of vitamin D on the content of surfactant protein still needs further research to confirm the long-term impact.…”