Xiping Liao ^# 1 2, Ji Liu ^# 3, Xiaolong Guo ¹, Ruiping Meng ¹, Wei Zhang ¹, Jianyun Zhou ¹, Xia Xie ^1 2, Hongli Zhou ¹

J Inflamm Res. 2024 May 13:17:2897-2914. doi: 10.2147/JIR.S450801. eCollection 2024.

Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic disease resulting from the interaction of various factors such as social elements, autoimmunity, genetics, and gut microbiota. Alarmingly, recent epidemiological data points to a surging incidence of IBD, underscoring an urgent imperative: to delineate the intricate mechanisms driving its onset. Such insights are paramount, not only for enhancing our comprehension of IBD pathogenesis but also for refining diagnostic and therapeutic paradigms. Monocytes, significant immune cells derived from the bone marrow, serve as precursors to macrophages (Mφs) and dendritic cells (DCs) in the inflammatory response of IBD. Within the IBD milieu, their role is twofold. On the one hand, monocytes are instrumental in precipitating the disease’s progression. On the other hand, their differentiated offsprings, namely moMφs and moDCs, are conspicuously mobilized at inflammatory foci, manifesting either pro-inflammatory or anti-inflammatory actions. The phenotypic spectrum of these effector cells, intriguingly, is modulated by variables such as host genetics and the subtleties of the prevailing inflammatory microenvironment. Notwithstanding their significance, a palpable dearth exists in the literature concerning the roles and mechanisms of monocytes in IBD pathogenesis. This review endeavors to bridge this knowledge gap. It offers an exhaustive exploration of monocytes’ origin, their developmental trajectory, and their differentiation dynamics during IBD. Furthermore, it delves into the functional ramifications of monocytes and their differentiated progenies throughout IBD’s course. Through this lens, we aspire to furnish novel perspectives into IBD’s etiology and potential therapeutic strategies.

Shigaku Ikeda ¹, Hidetoshi Takahashi ², Yasushi Suga ³, Hikaru Eto ⁴, Takafumi Etoh ⁵, Keiko Okuma ⁶, Kazuo Takahashi ⁷, Takeshi Kanbara ⁸, Mariko Seishima ⁹, Akimichi Morita ¹⁰, Yasutomo Imai ¹¹, Takuro Kanekura ¹²

J Am Acad Dermatol 2013 Apr;68(4):609-617. doi: 10.1016/j.jaad.2012.09.037. Epub 2013 Jan 17.

Background: Generalized pustular psoriasis (GPP) is a chronic autoimmune disease characterized by fever, erythema, and neutrophilic pustules over large areas of the skin. GPP does not respond well to pharmacologic intervention. Objective: We sought to assess efficacy of selectively depleting the myeloid lineage leukocytes in patients with GPP. Methods: Fifteen patients with persistent moderate to severe GPP despite conventional therapy were included. Eligible patients had more than 10% of their skin area covered by pustules. Treatment with oral etretinate, cyclosporine, methotrexate, prednisolone, and topical prednisolone/vitamin D3 was continued if had been initiated well in advance of study entry. Five sessions of adsorptive granulocyte and monocyte apheresis (GMA) with the Adacolumn (JIMRO Co Ltd, Takasaki, Japan) were administered (1 session/wk over 5 weeks) to selectively deplete Fcγ receptor and complement receptor bearing leukocytes. Efficacy was assessed by measuring the skin areas covered by pustules at baseline and 2 weeks after the last GMA session. Results: One patient did not complete the first GMA session. Based on the GPP severity scores relative to entry, the overall scores improved (n = 14, P = .0027), and the area of erythroderma (P = .0042), pustules (P = .0031), and edema (P = .0014) decreased. Likewise, Dermatology Life Quality Index improved (P = .0016), reflecting better daily function and quality of life. Twelve patients were judged as responders (85.7%), and 10 patients maintained the clinical response for 10 weeks after the last GMA session without any change in medication. Limitations: This study was unblinded and without a placebo arm. Conclusion: GMA in this clinical setting was safe and effective, suggested a major role for granulocytes/monocytes in the immunopathogenesis of GPP.

https://pubmed.ncbi.nlm.nih.gov/23332516/