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\begin{document}

\title{Adiponectin inhibits the production of TNF-alpha, IL-6 and chemokines by
human lung macrophages}



\author[1]{Helene Salvator}%
\author[2]{Stanislas Grassin-Delyle}%
\author[2]{Marion Brollo}%
\author[2]{Louis-jean Couderc}%
\author[2]{Charlotte Abrial}%
\author[2]{Tatiana Victoni}%
\author[2]{Emmanuel Naline}%
\author[2]{Philippe Devillier}%
\affil[1]{Viorologie Immunologie Moleculaire (VIM) Suresnes - V2I- UMR 0892}%
\affil[2]{Virologie et Immunologie Moleculaire (VIM) Suresnes, V2I - UMR-0892}%


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  \date{June 15, 2024}


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\begin{abstract}
Background and purpose: Obesity is associated with an elevated risk of
severe respiratory infections and inflammatory lung diseases. The
objectives were to investigate (i) the production of adiponectin by
human lung explants, (ii) the expression of the adiponectin receptors
AdipoR1 and AdipoR2 by human lung macrophages (LMs), and (iii) the
impact of recombinant human adiponectin and a small-molecule APN
receptor agonist (AdipoRon) on LMs activation. Experimental approach:
Human parenchyma explants and LMs were isolated from patients operated
for carcinoma. The LMs were cultured with recombinant adiponectin or
AdipoRon and stimulated with LPS (10 ng.mL-1), poly(I:C) (10 \selectlanguage{greek}µ\selectlanguage{english}g.mL-1) or
interleukin(IL)-4 (10 ng.mL-1) for 24 h. Cytokines or adiponectin,
released by explants or LMs, were measured using ELISAs. The mRNA levels
of AdipoR1 and AdipoR2 were determined using real-time quantitative PCR.
AdipoRs expression was also assessed with confocal microscopy. Key
results: Adiponectin was released by lung explants at a level negatively
correlated with the donor's body mass index. AdipoR1 and AdipoR2 were
both expressed in LMs. Adiponectin (3-30 \selectlanguage{greek}µ\selectlanguage{english}g.mL-1) and AdipoRon (25-50
\selectlanguage{greek}μ\selectlanguage{english}M) markedly inhibited the LPS- and poly(I:C)-induced release of Tumor
Necrosis Factor-alpha, IL-6 and chemokines (CCL3, CCL4, CCL5, CXCL1,
CXCL8, CXCL10) and the IL-4-induced release of chemokines (CCL13, CCL17,
CCL22) in a concentration-dependent manner. Recombinant adiponectin
produced in mammalian cells (lacking low molecular weight isoforms) had
no effects on LMs. Conclusions and implications: The
low-molecular-weight isoforms of adiponectin and AdipoRon have an
anti-inflammatory activity in the lung environment. Targeting
adiponectin receptors may constitute a new means of controlling airways
inflammation.%
\end{abstract}%



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\includegraphics[width=0.70\columnwidth]{figures/Fig4-APN-MP/Fig4-APN-MP}

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