Abstract
Gender differences in pulmonary inflammation have been well documented. Although low molecular mass hyaluronan (LMMHA) is known to trigger pulmonary lung inflammation, sex differences in susceptibility to LMMHA are still unknown. In this study, we test the hypothesis that mice may display sex-specific differences after LMMHA administration. After LMMHA administration, male mice have higher neutrophil, cytokine, and chemokine counts compared to that of their female counterparts. Additionally, Ovariectomized (OVX) mice show greater LMMHA-induced inflammation compared to that of mice with intact ovaries. Injections of OVX mice with 17β-estradiol can decrease inflammatory responses in the OVX mice. These results show that ovarian hormones regulate LMMHA induced lung inflammation.
Highlights
Hyaluronan, or hyaluronic acid (HA), is a major component of an extracellular matrix with a structure made up of polymeric disaccharides D-Glucuronic acid and N-acetyl-Dglucosamine A linked by glucuronic acid bonds [1]
We reported that intratracheal administration of low-molecular-mass HA (LMMHA) (200 kDa) causes neutrophil infiltration in mice lungs, which is associated with an increase in interleukin-6 (IL-6), chemokine (C-X-C motif) ligand 1 (CXCL-1), tumor necrosis factor-α (TNF-α), and chemokine (C-X-C motif) ligand
To determine the role of estrogen in lung inflammation, we evaluated if E2 can mimic regulatory functions of ovariectomized mice in acute lung injury
Summary
Hyaluronan, or hyaluronic acid (HA), is a major component of an extracellular matrix with a structure made up of polymeric disaccharides D-Glucuronic acid and N-acetyl-Dglucosamine A linked by glucuronic acid bonds [1]. Rapid degradation of hyaluronic acid produces low-molecular-mass HA (LMMHA), which has pro-inflammatory effects and acts as an intracellular signal molecule in inflammation [2]. Patients with acute respiratory distress syndrome, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and asthma have significantly increased LMMHA [3,4,5,6]. LMMHA upregulates adhesion molecules in endothelial cells and induces production of pro-inflammatory cytokines in airway epithelial cells [7]. In vitro studies have shown that in response to LMMHA stimulation, macrophages are the main effector cells in producing pro-inflammatory chemokines and cytokines [7]. We reported that intratracheal administration of LMMHA (200 kDa) causes neutrophil infiltration in mice lungs, which is associated with an increase in interleukin-6 (IL-6), chemokine (C-X-C motif) ligand 1 (CXCL-1), tumor necrosis factor-α (TNF-α), and chemokine (C-X-C motif) ligand
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