Immunopathology of trachomatous conjunctivitis.

Abstract

Upper palpebral conjunctival biopsy specimens obtained from eight patients with active trachoma were examined by routine histological and immunohistochemical methods. The epithelium expressed class I major histocompatibility complex (MHC) products throughout and class II MHC products in the superficial layers. The epithelial inflammatory infiltrate consisted of polymorphonuclear leucocytes, macrophages, T lymphocytes, and dendritic cells. In the underlying stroma the inflammatory infiltrate was organised as B lymphoid follicles, and there was also a diffuse infiltrate consisting of plasma cells and scattered B lymphoid cells, dendritic cells, T cells, macrophages, and polymorphonuclear leucocytes. Each type of cell has its special location in the tissue. Plasma cells were located on a subepithelial band and as a dense infiltrate round the acini of accessory lacrimal glands. IgA+ plasma cells outnumbered IgG+ cells, whereas IgM+ and IgE+ cells were few. Our data provide good evidence for the presence of both humoral and cell mediated immune responses and a possible role for autoimmune mechanisms in the conjunctival tissues of trachoma patients.

Expression of growth factors in the conjunctiva from patients with active trachoma

“…2,4 Briefly, the inflammatory infiltrate in the epithelium consisted of large numbers of macrophages, T lymphocytes, polymorphonuclear leucocytes, and dendritic cells. The stromal inflammatory infiltrate was organized as lymphoid follicles and as a diffuse infiltrate.…”

“…In previous immunohistochemical studies, we demonstrated the presence of increased numbers of activated macrophages in the conjunctival biopsy specimens from patients with active trachoma. 2,3 These macrophages showed cytoplasmic expression of the fibrogenic cytokines interleukin-1a, interleukin-1b, tumor necrosis factor-a, and platelet derived growth factor. 3 In the normal conjunctiva, there was no immunoreactivity for CTGF and bFGF.…”

“…However, in previous immunohistochemical studies we have demonstrated that the tissue damage might result from immunological mechanisms involving T lymphocytes, macrophages, gelatinase B, and cytokines released by resident conjunctival cells, and by inflammatory cells infiltrating the tissue. [2][3][4] Growth factors regulate many of the processes crucial for normal repair after tissue injury, including chemotactic migration of inflammatory cells and fibroblasts, mitosis of cells, neovascularization, and synthesis of extracellular matrix (ECM) components. 5,6 However, prolonged production of these cytokines can lead to excessive matrix accumulation and chronic fibrosis, often resulting in loss of tissue structure and function.…”

Trachoma as cause of blindness: literature review

“…It begins in the form of follicular conjunctivitis (active follicular trachoma), with papillary hypertrophy and inflammatory cells infiltrating the conjunctiva (lymphocytes, macrophages, neutrophils, and plasma cells) punctuated by lymphoid follicles (B cells surrounded by a mantle of T0 cells ) [23], which extends throughout the conjunctiva, especially in the upper tarsal conjunctiva.…”

Reorganization of the host cytoskeleton by the intracellular pathogenChlamydia trachomatis

“…7 We propose that chlamydial modulation of host cytoskeleton may constitute a mechanism of immune-modulation. Because tissue damage in the form of scarring of genital, ocular or bronchial mucosal epithelia is due mostly to inflammation, 19,20 a detailed understanding of factors governing pathogenic vacuole stability will offer new insights into the interaction of Chlamydiae with host innate immune pathways.…”