Type 2 diabetes mellitus (T2D) is a risk factor for the development of tuberculosis (TB) through mechanisms poorly understood. Monocytes and macrophages are key effector cells to control TB, but they are also subverted by Mycobacterium tuberculosis (Mtb). Specifically, Mtb can induce a bystander effect that skews monocyte differentiation towards macrophages with a permissive phenotype to infection. Here, we evaluated whether T2D impacts this TB aspect. Our approach was to differentiate monocytes from healthy control (HC) subjects and T2D patients into macrophages (MDM), and then assess their response to Mtb infection, including their secretome content and bystander effect capacity. Through flow cytometric analyses, we found a lower level of activation markers in MDM from T2D patients than from HC in response to mock (HLA‐DR, CD86 and CD163) or Mtb challenge (CD14 and CD80). In spite of high TGF‐β1 levels in mock‐infected MDM from T2D patients, cytometric bead arrays indicated that there were no major differences in the secretome cytokine content in these cells relative to HC‐MDM, even in response to Mtb. Mimicking a bystander effect, the secretome of Mtb‐infected HC‐MDM drove HC monocytes towards MDM with a permissive phenotype for Mtb intracellular growth. However, the secretome from Mtb‐infected T2D‐MDM did not exacerbate the Mtb load compared to secretome from Mtb‐infected HC‐MDM, possibly due to the high IL‐1β production relative to Mtb‐infected HC‐MDM. Collectively, despite T2D affecting the basal MDM activation, our approach revealed that it has no major consequence on their response to Mtb or capacity to generate a bystander effect influencing monocyte differentiation.
Introduction: Vogt-Koyanagi-Harada disease is a systemic autoimmune disease characterized mainly by a bilateral granulomatous panuveitis, in which antibodies are produced against tissues rich in melanocytes such as the retina, inner ear, meninges, skin, and hair, which explains its extraocular manifestations and its clinical presentation. Case report: A 27-year-old Mexican woman presented with sudden reduced visual acuity, with no history of trauma or eye surgery, without evidence of another ocular disease, she also presented meningism and disacusia. Retinal detachment is evidenced with the help of imaging studies, in addition to cerebrospinal fluid pleocytosis. The final diagnosis during her stay in the hospital was VKH disease. Discussion: The clinical case presented, based on current criteria for the diagnosis and classification of VKH disease is an incomplete VKH, and it was not possible to demonstrate the dermatological involvement in future stages to classify it as a complete VKH disease. Conclusion: VKH disease is difficult to diagnose, because its diagnostic criteria are mainly exclusion and its clinical presentation is variable and insidious, which results in a generally late diagnosis and treatment, allowing the appearance and progression of sequelae. Possibly, the diagnostic criteria for VKH disease should be subjected to a new review, to specify the most frequent clinical data in recent years, since they were published almost a couple of decades ago.
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