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Biomedical subjects

Miriam Pietrzyk

Publications and source records attributed to Miriam Pietrzyk.

5 recordsLinked to original sources
PubMed2006

Expression of the chemokine receptor CXCR3 in human renal allografts--a prospective study.

BACKGROUND: Mechanisms involved in the recruitment and activation of inflammatory cells during renal allograft injury are still incompletely understood. Since chemokines play pivotal roles in this process, our prospective study was performed to evaluate further the role of the chemokine receptor CXCR3. METHODS: A total of 138 biopsies were included from patients without rejection and unaltered morphology (according to Banff 97 classification grade 1, n = 49), with acute interstitial rejection (Banff grade 4 type I, n = 8), with acute vascular rejection (Banff grade 4 type II, n = 23), with chronic allograft nephropathy (Banff grade 5, n = 16), without rejection but with various other lesions (Banff grade 6, n = 36) and from pre-transplant kidneys (n = 6). The expression of CXCR3-, CD4- and CD8-positive cells was localized by immunohistochemistry and quantified by image analysis. RESULTS: CXCR3 was expressed by infiltrating inflammatory cells, but not by intrinsic renal structures. CXCR3-positive cells were found to be involved in tubulitis and vascular rejection. The area of CXCR3-positive staining was significantly larger in biopsies with acute interstitial rejection (P<0.001) and acute vascular rejection (P<0.001) as compared with normal renal graft biopsies. There was a strong morphological and numerical correlation between CXCR3 and both CD4- and CD8-positive T cells, respectively. CONCLUSIONS: A significant part of both CD4- and CD8-positive T cells express the chemokine receptor CXCR3. During renal allograft rejection, the number of these cells increases significantly at the site of injury and might be targeted by CXCR3 blocking agents.

Biomarkers↗
PubMed2006

Expression of cyclooxygenase-1 and cyclooxygenase-2 in human renal allograft rejection-- a prospective study.

Cyclooxygenases (COX) are known to be involved in inflammatory kidney diseases. However, there are no data available about the expression of COX-1 and only preliminary reports about the expression of COX-2 in biopsies of patients undergoing acute renal allograft rejection. We conducted this prospective study to analyze the expression, distribution, and cellular localization of COX-1 and -2 and thus to elucidate the role of COX in human kidney transplantation. One hundred forty-four biopsies were included from patients without rejection and unaltered morphology (n = 60), with acute interstitial rejection (n = 7), with acute vascular rejection (n = 21), with chronic allograft nephropathy (n = 16), without rejection but with various other lesions (n = 40). COX-1 and -2 expression was localized in each biopsy by immunohistochemistry. We found a highly significant up-regulation of COX-1 in vessels and in infiltrating interstitial cells of patients with acute allograft rejection compared with biopsies with well-preserved tissue. Also, COX-2 expression was significantly elevated in infiltrating interstitial cells of biopsies with acute rejection. This is the first prospective study demonstrating a significant induction of both COX-1 and -2 in human allograft biopsies with acute rejection after renal transplantation.

Adult↗
PubMed2005

Solid-organ transplantation in HBsAg-negative patients with antibodies to HBV core antigen: low risk of HBV reactivation.

Hepatitis B virus (HBV) reactivation is a well-described event in HBV surface antigen (HbsAg)-positive patients undergoing immunosuppression. There are only few data about the risk of HBV reactivation in HBsAg-negative solid-organ transplant recipients with resolved HBV infection. We conducted a systematic screening of serum and liver samples from 38 HBsAg-negative and anti-HBV core antigen (anti-HBc)-positive patients for the presence of HBV-DNA and for serologic HBV markers before and after solid-organ transplantation (kidney, n=23; liver, n=9; heart, n=6). Pretransplant prevalence of HBV-DNA was 24% (6/25) in serum and 33% (3/9) in liver samples. Forty-four percent (15/34) of the recipients were viremic after transplantation; this finding was more common in patients coinfected with hepatitis C (P=0.011) and in patients negative for anti-HBs (P=0.001). Two recipients became antigenemic (HBsAg-positive), but none developed clinical signs of hepatitis. In conclusion, subclinical reactivation of HBV infection was detected in a significant proportion of HBsAg-negative solid-organ-transplant recipients.

Antibodies, Viral↗