COX-2 expression in stromal fibroblasts self-limits their numbers in lymph node inflammatory responses

Area of Science:

• Immunology
• Cell Biology
• Histology

Background:

• Cyclooxygenase (COX)-2 expression was previously reported in draining lymph nodes during carrageenin-induced pleurisy in rats.
• The specific cell types and characteristics of COX-2 expressing cells in this inflammatory model remained to be elucidated.

Purpose of the Study:

• To investigate the histological and immunohistochemical features of cyclooxygenase (COX)-2 expressing cells in draining lymph nodes during carrageenin-induced pleurisy in rats.
• To identify the cell lineage and functional role of COX-2 expressing cells in the context of lymph node inflammation and remodeling.

Main Methods:

• Carrageenin was administered into the pleural cavity of rats to induce pleurisy.
• Parathymic lymph nodes were collected at various time points post-injection (8h, 16h, 24h, 48h).
• Histological and immunohistochemical analyses were performed to identify COX-2 expressing cells and co-localize them with specific cell markers (α-smooth muscle actin, desmin).

Main Results:

• Carrageenin induced significant enlargement of parathymic lymph nodes, with peak enlargement observed between 24 and 48 hours.
• Lymphatic follicles disappeared by 16 hours, and macrophages and fibroblasts became prominent in the cortical region.
• COX-2 expressing cells exhibited dendritic processes from 16 to 48 hours and co-localized with α-smooth muscle actin (α-SMA) and desmin, markers for stromal fibroblastic reticular cells.
• Expression of α-SMA increased following COX-2 expression.
• Treatment with nimesulide, a COX-2 inhibitor, enhanced the dendritic processes of COX-2 expressing cells and increased the expression of both COX-2 and α-SMA.

Conclusions:

• The results suggest that COX-2 expressing cells in draining lymph nodes during carrageenin-induced pleurisy are likely stromal fibroblastic cells.
• These COX-2 expressing stromal cells may play a role in the negative self-regulation of their proliferation.
• These cells appear to modulate the tissue remodeling processes within draining lymph nodes at sites of inflammation.