Thymopoietic and Bone Marrow Response to Murine Pneumocystis Pneumonia

Shi, Xiaorui; Zhang, Ping; Sempowski, Gregory D.; Shellito, Judd E.

doi:10.1128/iai.01213-10

Cited by 16 publications

(18 citation statements)

References 57 publications

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“…Interestingly, these and other studies seem to suggest that the thymus may play a role in maintaining immune efficacy in the adult (21). Indeed, reports, using mice, have demonstrated the need for the continual production of naïve T cells to mount an effective immune response against bacterial (24), viral (25), and fungal infections (26); with the latter study showing that mice thymectomized at 5 weeks of age exhibited a delayed response to Pneumocystis infection. Furthermore, amongst HIV-infected patients under highly active antiretroviral therapy, those individuals that show enhanced T cell output appear to demonstrate a better prognosis (27, 28).…”

Section: The Impact Of Thymic Involution On Peripheral T Cell Senescencementioning

confidence: 99%

The Effect of Age on Thymic Function

Palmer¹

2013

Front. Immunol.

378

296

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Age-related regression of the thymus is associated with a decline in naïve T cell output. This is thought to contribute to the reduction in T cell diversity seen in older individuals and linked with increased susceptibility to infection, autoimmune disease, and cancer. Thymic involution is one of the most dramatic and ubiquitous changes seen in the aging immune system, but the mechanisms which underlying this process are poorly understood. However, a picture is emerging, implicating the involvement of both extrinsic and intrinsic factors. In this review we assess the role of the thymic microenvironment as a potential target that regulates thymic involution, question whether thymocyte development in the aged thymus is functionally impaired, and explore the kinetics of thymic involution.

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Section: The Impact Of Thymic Involution On Peripheral T Cell Senescencementioning

confidence: 99%

The Effect of Age on Thymic Function

Palmer¹

2013

Front. Immunol.

378

296

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“…For example, during malaria and toxoplasmosis (and other systemic challenges), there is an increase in granulocytes in the BM, but a transient decrease in the numbers of lymphocytes, erythrocytes, and megakaryocytes, despite low parasite burdens in this site (21–24). Increased populations of LSKs and/or HSCs in the BM are the hallmark of many experimental infections (25–31). Thus, challenge with Plasmodium chabaudi or Pneumocystis carinii , organisms not typically found in the BM, leads to increased LSK and HSC populations in the BM and circulation, followed by an increase in multipotent progenitor cells (25, 26).…”

Section: Inflammation Infection and Hematopoiesismentioning

confidence: 99%

“…Increased populations of LSKs and/or HSCs in the BM are the hallmark of many experimental infections (25–31). Thus, challenge with Plasmodium chabaudi or Pneumocystis carinii , organisms not typically found in the BM, leads to increased LSK and HSC populations in the BM and circulation, followed by an increase in multipotent progenitor cells (25, 26). Similarly, murine ehrlichiosis results in increased numbers of LSK cells, though these cells appear to have a defect in their ability to differentiate (32, 33).…”

Section: Inflammation Infection and Hematopoiesismentioning

confidence: 99%

Infection-Induced Changes in Hematopoiesis

Zaretsky

Engiles²,

Hunter

2014

The Journal of Immunology

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The bone marrow is an important site for the interrelated processes of hematopoiesis, granulopoiesis, erythropoiesis and lymphopoiesis. A wide variety of microbial challenges are associated with profound changes in this compartment that impact on hematopoietic differentiation and mobilization of a variety of cell types. This article reviews some of the key pathways that control BM homeostasis, the infectious and inflammatory processes that affect the BM, and how addressing the knowledge gaps in this area has the potential to widen our comprehension of immune homeostasis.

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“…However, pDCs can be recruited to inflamed lymph nodes and once mature, pDCs can efficiently stimulate naïve T cells 12) . Also in previous report, chemokine receptor CCR9 was induced by TLR9 activation 13) . CCR9 is a key regulator of leukocyte migration and CCR9 + pDCs are potent inducers of Tregs 14) .…”

Section: Introductionmentioning

confidence: 69%

Imiquimod-induced CCR9 Ameliorates murine TNBS Colitis

Suzuki¹,

Katakura²,

Fujiwara³

et al. 2016

FJMS

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AIMS :To investigate whether Imiquimod (IMQ) as TLR7 ligand protects mice from colonic inflammation and the mechanisms underlying in such immunoregulatory conditions. METHODS : Murine colitis was induced to Balb/c mice by administration of trinitrobenzene sulfonic acid (TNBS) with or without daily intraperitoneal administration of IMQ. Colitis was evaluated by body weight decreases and by histological score. Also colonic mRNA expression was measured by RT -PCR. To confirm the induction of Regulatory T cells (Tregs) by type -1 IFN from pDCs, we generated mouse bone marrow -derived pDCs and co -cultured these with CD4 + T cells isolated from mouse spleen with or without IMQ stimulation. Cytokine production in the culture supernatant was measured by ELISA and the number of Tregs were analyzed by flow cytometry. Spleen and mesenteric lymph nodes (MLN) from IMQ -treated mice were collected, and mRNA expressions of cytokine were measured by RT -PCR and cytokine productions were measured by ELISA. Tregs and chemokine expressions were analyzed in colon of TNBS -induced colitis mouse by immunohistochemistry. RESULTS : Administration of IMQ significantly suppressed colonic inflammation of TNBS -induced colitis. In the colons of IMQ -treated mice, mRNA expression of TNF -α was decreased, and strong expressions of IL -6, IFN -β and TGF -β were detected. IL -10 and TGF -β productions were increased in the supernatant of co -cultured cells stimulated with IMQ, although we were unable to detect Treg differentiaton in IMQ -stimulated co -cultured cells. In MLN of IMQ -treated mice, strong expressions of TLR7, IFN -β, TGF -β and Foxp3 mRNA were detected. IL -10 production from MLN cells was also increased in the IMQ -treated group. Finally, Tregs in the inflamed colon and CCR9 in MLN of IMQ -treated mice were detected. CONCLUSION : These results suggest that IMQ protects mice from TNBS colitis through induction of CCR9, which regulates accumulation of Tregs in the inflamed colon.

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Thymopoietic and Bone Marrow Response to Murine Pneumocystis Pneumonia

Cited by 16 publications

References 57 publications

The Effect of Age on Thymic Function

The Effect of Age on Thymic Function

Infection-Induced Changes in Hematopoiesis

Imiquimod-induced CCR9 Ameliorates murine TNBS Colitis

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