Aspirin and immune system

Hussain, Muzammal; Javeed, Aqeel; Ashraf, Muhammad; Zhao, Yong; Mukhtar, Muhammad Mahmood; Rehman, Mujeeb ur

doi:10.1016/j.intimp.2011.11.021

Cited by 72 publications

(57 citation statements)

References 155 publications

(161 reference statements)

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“…32 For T lymphocytes, aspirin can disrupt the integrin- and SELL (selectin L)-mediated binding of T cells to the endothelium, 33, 34 directly suppress T cell activation or proliferation, and/or inhibit cytokine production related to the T cell-mediated adaptive immune response. 25 Our data support the possibility that aspirin may cooperate with the host immune system, in particular, lymphocytes, to interrupt the development or growth of colorectal neoplasia.…”

Section: Discussionsupporting

confidence: 74%

“…Evidence suggests that aspirin may exert multiple effects on different components of innate and adaptive immunity through modulation of immune and inflammatory cytokines. 23, 25–29 For example, aspirin may induce tolerogenic activity in dendritic cells and inhibit their subsequent immunostimulatory function. 30 In addition, aspirin can induce apoptosis in neutrophils and monocytes, 31 and trigger a lipoxin-driven immune counter-regulation.…”

Section: Discussionmentioning

confidence: 99%

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Regular Aspirin Use Associates With Lower Risk of Colorectal Cancers With Low Numbers of Tumor-Infiltrating Lymphocytes

et al. 2016

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Background & Aims Aspirin use reduces colorectal cancer risk. Aspirin, a nonsteroidal anti-inflammatory drug, inhibits PTGS2 (cyclooxygenase-2); PTGS2 promotes inflammation and suppresses T cell-mediated adaptive immunity. We investigated whether the inverse association of aspirin use with colorectal carcinoma risk was stronger for tumors with lower degrees of lymphocytic infiltrates than for tumors with higher degrees of lymphocytic infiltrates. Methods We collected aspirin use data biennially from participants in the Nurses’ Health Study and Health Professionals Follow-up Study. Participants were asked whether they took aspirin in most weeks, the number of tablets taken per week, and years of aspirin use. We collected available tumor specimens (n=1458) from pathology laboratories in the US. A pathologist confirmed the diagnosis of colorectal adenocarcinoma (excluding anal squamous cell carcinoma), and evaluated histopathology features, including patterns and degrees of lymphocytic infiltrates within and around tumor areas. Person-years of follow-up were accrued from the date of return of questionnaires until dates of colorectal cancer diagnosis, death, or the end of follow-up (June 2010). Duplication-method Cox proportional hazards regression was used to assess the association of aspirin with incidence of colorectal carcinoma subgroups according to the degree of tumor-infiltrating lymphocytes (TILs), intratumoral periglandular reaction, peritumoral reaction, or Crohn’s-like reaction. Results We documented 1458 rectal and colon cancers. The inverse association between regular aspirin use and colorectal cancer risk significantly differed by concentrations of TILs (Pheterogeneity =0.007). Compared with nonregular use, regular aspirin use was associated with a lower risk of tumors that had low levels of TILs (relative risk, 0.72; 95% CI, 0.63–0.81); strength of the association depended on aspirin dose and duration (both Ptrend <0.001). In contrast, aspirin use was not associated with a risk of tumors having intermediate or high levels TILs. This differential association was consistent regardless of status of tumor microsatellite instability, mutations in BRAF, or expression of PTGS2. Regular aspirin use was associated with a lower risk of tumors that contained low levels of CD3+ T cells, CD8+ T cells, or CD45RO (PTPRC)+ T cells (measured by immunohistochemistry and computer-assisted image analysis). Conclusions Based on data from the prospective cohort studies, regular use of aspirin is associated with a lower risk of colorectal carcinomas with low concentrations of TILs. These findings indicate that the immune response in the tumor microenvironment could be involved in the chemopreventive effects of aspirin.

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Section: Discussionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Regular Aspirin Use Associates With Lower Risk of Colorectal Cancers With Low Numbers of Tumor-Infiltrating Lymphocytes

et al. 2016

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“…29,36 Aspirin is generally considered to have immunesuppressive capabilities. 42 Clinical administration of aspirin has beneficial effects on certain autoimmune diseases, 43 as well as allograft rejection. 44 Aspirin and other nonsteroidal anti-inflammatory drugs were reported to suppress the humoral immune response by impairing antibody synthesis.…”

Section: Discussionmentioning

confidence: 99%

COX-1–derived thromboxane A2 plays an essential role in early B-cell development via regulation of JAK/STAT5 signaling in mouse

Yang

Shi

Shen

et al. 2014

Blood

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• This study demonstrated an essential role of COX-1 in early B-cell development.• Low-dose aspirin may have a potential suppressive effect on B-cell development in humans.Cyclooxygenases (COXs) and their prostanoid products play important roles in a diverse range of physiological processes, including in the immune system. Here, we provide evidence that COX-1 is an essential regulator in early stages of B-cell development. COX-1-deficient mice displayed systematic reduction in total B cells, which was attributed to the arrest of early B-cell development from pro-B to pre-B stage. We further demonstrated that this defect was mediated through downregulation of the Janus kinase/signal transducer and activator of transcription 5 (JAK/STAT5) signaling and its target genes, including Pax5, in COX-1 2/2 mice. Mechanistic studies revealed that COX-1-derived thromboxane A 2 (TxA 2 ) could regulate JAK3/STAT5 signaling through the cyclic adenosine monophosphate-protein kinase A pathway, via binding with its receptor thromboxane A2 receptor (TP). Administration of the TP agonist could rescue the defective B-cell development and JAK/STAT5 signaling activity in COX-1-deficient mice. Moreover, administration of low-dose aspirin caused a significant reduction in total B cells in peripheral blood of healthy human volunteers, coincidentally with reduced TxA 2 production and downregulation of JAK/STAT5 signaling. Taken together, our results demonstrate that COX-1-derived TxA 2 plays a critical role in the stage transition of early B-cell development through regulation of JAK/STAT5 signaling and indicate a potential immune-suppressive effect of low-dose aspirin in humans. (Blood. 2014;124(10):1610-1621

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“…There has been conflicting reports regarding the effect of lowdose aspirin on the hemodynamic condition of uterus (24)(25)(26)(27)). There has not been any comprehensive studies regarding the immunomodulatory role of aspirin on the NK cells of body tissues (28). In addition, there are conflicting reports regarding the effect of aspirin on the NK cells of other tissues.…”

Section: Introductionmentioning

confidence: 99%

“…These variations indicate that more research is needed to understand the effect of aspirin on the NK cells in different tissues (28). Based on the studies, low dosage of aspirin results in an alteration in the levels of ovarian steroidal hormones; however, the aspirin regulatory role in the NK cells in different tissues has not been investigated yet.…”

Section: Introductionmentioning

confidence: 99%

Low-Dose Aspirin and Uterine Natural Killer Cells in Mice at Day Seven of Pregnancy

Boroujeni

Gholami

et al. 2015

Jentashapir J Health Res

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Background: Inhibiting the effect of aspirin on prostaglandin results in corpus luteum maintenance in pregnant mice. Uterine natural killer (uNK) cells activate between 5 -7 days of pregnancy. uNK cell differentiation is indirectly regulated by ovarian hormones. Immune cells have important roles in the endometrium at early pregnancy stages. Although low-dose aspirin is effective on ovarian hormones, the effect of low-dose aspirin on the uNK cell population at early pregnancy stages is unknown. Objectives: The aim of this study was to assess the effect of low-dose aspirin on uNK cells at day seven of pregnancy. Materials and Methods: Adult female mice were coupled and divided into two groups (control and experimental). Thereafter, mice in the experimental group received 7.5 mg/kg aspirin twice a day for one week. Blood samples were collected for the measurement of the level of ovarian hormones at day seven of pregnancy and finally the animals were sacrificed by cervical dislocation and uterine horns were removed for histological study. Periodic acid-schiff (PAS) staining was performed for uNK cell counting. Data analysis was conducted by SPSS software. Results: The ovarian hormones level showed a significant difference between the experimental and control groups (P < 0.05). Furthermore, the uNK cell population showed a significant difference between the two groups (P < 0.05). Conclusions: Increased ovarian hormones due to low-dose aspirin administration resulted in decline in the uNK cells number, which may be effective in successful pregnancy.

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Aspirin and immune system

Cited by 72 publications

References 155 publications

Regular Aspirin Use Associates With Lower Risk of Colorectal Cancers With Low Numbers of Tumor-Infiltrating Lymphocytes

Regular Aspirin Use Associates With Lower Risk of Colorectal Cancers With Low Numbers of Tumor-Infiltrating Lymphocytes

COX-1–derived thromboxane A2 plays an essential role in early B-cell development via regulation of JAK/STAT5 signaling in mouse

Low-Dose Aspirin and Uterine Natural Killer Cells in Mice at Day Seven of Pregnancy

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