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Biomedical subjects

C Höflich

Publications and source records attributed to C Höflich.

7 recordsLinked to original sources
PubMed2005

[Impact of pneumoperitoneum on expression of E-cadherin, CD44v6 and CD54 (ICAM-1) on HT-29 colon-carcinoma cells].

INTRODUCTION: The mechanism of potential tumor cell spread and growth during laparoscopy is poorly understood. Nevertheless, different experimental studies reported a stimulation of tumor cell growth and an increased metastatic potential of carcinoma cells using carbon dioxide as an insufflation medium. Adhesion molecules do play an important and regulatory function in the process of metastatic spread and invasion of cancer cells. Therefore we investigated the influence of CO2 and Helium insufflation on the in-vitro expression of E-Cadherin, CD44v6 and CD54 (ICAM-1) on HT-29 colon carcinoma cells. METHODS: HT-29 carcinoma cells were exposed to either CO2 or helium insufflation. Expression of E-Cadherin, CD44v6 and CD54 (ICAM-1) on HT-29 colon carcinoma cells were measured 1, 12, 24, 48 and 96 h after CO2 and helium insufflation using flowcytometry (FACScan). Data were analyzed by Friedman-test. RESULTS: HT-29 cell line showed a short decrease in E-Cadherin expression after CO2 exposure while helium insufflation had no influence. In contrasts to these findings the expression of CD44v6 and CD54 on HT-29 cells were not influenced significantly by either CO2 or helium. CONCLUSION: CO2 seems only to have a minor influence on the expression of E-Cadherin while expression of other adhesion molecules did not change after CO2 incubation. The alternative gas helium did not cause any significant changes of the expression of either E-Cadherin, CD44v6 and CD54. Further investigations are needed to elucidate the changes of the metastatic potential of tumor cells after laparoscopic and open procedures.

Adenocarcinoma↗
PubMed2002

[Immunomodulation in sepsis].

INTRODUCTION: The systemic inflammatory response syndrome is induced by a strong inflammatory reaction which is called sepsis when it is caused by an infection. However, anti-inflammatory therapeutic strategies in septic patients were not successful, indicating a more complex system. It is now clear that systemic hyper-inflammation induces systemic anti- or hypo-inflammation which can lead to total paralysis of the immune system ("immunoparalysis"). METHODS: Several studies were performed to evaluate parameters for describing the patient's immunocompetence. Based on these parameters, pilot trials were initiated to test immunomodulating therapies depending on the patient's immunocompetence. RESULTS: The measurement of monocytic HLA-DR expression, as well as the measurement of ex vivo LPS-induced TNF-a secretion, are suitable to describe the patient's immunocompetence. In addition to classical inflammation markers, the characterization of the inflammatory and infection status is completed by measurement of the plasma cytokines, LBP and PCT. IFN-g or GM-CSF application as well as the removal of inhibitory plasma mediators by hemofiltration/plasmapheresis can reconstitute the immune function in patients with "immunoparalysis". CONCLUSIONS: Immunomodulating therapeutic strategies in septic patients have to orientate on the patient's immunocompetence and inflammatory as well as infectious status: a patient in a hyper-inflammatory phase may need anti-inflammatory therapy whereas a patient in "immunoparalysis" needs immunoreconstitution/immunostimulating therapy.

Adjuvants, Immunologic↗
PubMed2001

Massive elevation of procalcitonin plasma levels in the absence of infection in kidney transplant patients treated with pan-T-cell antibodies.

OBJECTIVE: To determine the value of procalcitonin (PCT) monitoring in transplant patients receiving pan-T-cell antibody therapy. DESIGN: Retrospective clinical study. SETTING: A collaborative study between the Institute of Medical Immunology, the Department of Nephrology and Internal Intensive Care, both Charite, Humboldt University Berlin, and the Department of Laboratory Medicine, Friedrichshain Hospital, Berlin, Germany. PATIENTS AND INTERVENTIONS: Thirty-one patients were included in the study: 8 kidney transplant patients with acute rejection episodes, 5 receiving OKT3 monoclonal antibody therapy, 3 receiving steroid bolus therapy; 21 patients undergoing renal transplantation, 11 receiving ATG perioperatively, 10 without ATG administration; 2 patients undergoing renal transplantation and receiving anti-IL-2R mAb. MEASUREMENTS AND RESULTS: Procalcitonin (PCT) and tumor necrosis factor (TNF) alpha plasma levels were measured in infection-free transplant patients treated with the pan-T-cell antibodies ATG or OKT3. We found PCT plasma concentrations up to 600 ng/ml (reference < 0.5 ng/ ml), which are comparable to those seen in severe sepsis. Increases in TNF-alpha plasma levels preceded the rises in PCT. After peaking on day 1 of therapy the PCT plasma concentrations returned to normal values independently of further antibody administration. In contrast, steroid bolus therapy or anti-interleukin 2 receptor mAb administration did not increase plasma PCT or TNF-alpha levels. CONCLUSIONS: PCT monitoring for evaluating infectious complications in kidney transplant patients must be very careful during pan-T-cell antibody therapy.

Antilymphocyte Serum↗
PubMed1998

CD45RA(bright)/CD11a(bright) CD8+ T cells: effector T cells.

An important aspect of peripheral T cell development is the differentiation from naive into memory cells. To distinguish naive from memory cells, CD45RA and CD11a are commonly used: CD45RA+ or CD11a(dim) T cells are regarded as naive, while CD45RA- or CD11a(bright) T cells are thought to be of memory type. There is, however, a CD8+ T cell subset which is CD45RA+ and at the same time CD11a(bright). It increases with age and in patients with systemic viral infections, though its functional role in the immune response is unknown. In the present study, we give evidence that this subset is related to memory-like T cells as it produces IFN-gamma and tumor necrosis factor-alpha, contains high levels of perforin, and expresses CD95 in the same way as memory-type CD45RA-/CD11a(bright) CD8+ T cells. Since it contains a high percentage of CD28- and CD57+ cells, is increased in size and granularity, and is transiently expressed following in vitro stimulation of naive CD8+ T cells, we speculate that this subset mainly represents recently activated effector T cells that are able to interact with CD80 and CD86 (B7-1 and B7-2 respectively) negative tissue cells.

Adult↗
PubMed1997

Selective in vivo deletion of alloactivated TH1 cells by OKT3 monoclonal antibody in acute rejection.

The OKT3 monoclonal antibody (mAb) recognizing the CD3 complex on human T-cells has been shown to be an effective immunosuppressive agent for the treatment and the prevention of acute rejection episodes in allograft recipients [1]. Following the initial doses of OKT3 mAb, activation of T lymphocytes and monocytes is observed. This is accompanied by a massive cytokine release, particularly following the first injection. The mAb opsonizes the circulating T-cells and the coated cells disappear quickly from circulation. OKT3 mAb is commonly administered for 5-10 days. The manifestation of side effects weeks (cytomegalovirus infection/disease, bacterial and fungal infections) or even months (Epstein-Barr-Virus related lymphoproliferative disease) after therapy as well as the good long-term effects on graft function suggest long-lasting immunosuppressive effects. Since peripheral T-cells reappear in the circulation already during therapy (with modulated CD3/T-cell receptor complex) and T-cell counts reach commonly pretreatment levels within 2-3 days after cessation of OKT3 mAb, the long-lasting immunosuppressive effects are not simply explainable by T-cell depletion. We wondered whether T-cells reappearing in the circulation after cessation of therapy, were functionally different from those before OKT3 mAb therapy. Our data suggest a selective depletion of activated T-cells particularly of type 1-like T-cells by OKT3 mAb resulting in long-lasting immune deviation that may explain the long-term effects of OKT3 mAb treatment.

Clonal Deletion↗
PubMed1996

Topical therapy of allergic rhinitis in childhood: Allergodil nasal spray--non-sedating in children.

The efficacy and safety of the nasally administered drug Allergodil in the treatment of allergic rhinitis were evaluated in a prospective drug monitoring programme conducted in Germany. Data from 489 children under the age 13 were included. The study was designed to gain knowledge about Allergodil in a normal clinical setting. Dosing was at the judgement of the investigator bearing in mind data sheet recommendations, i.e. one spray-puff (0.14 mg) per nostril twice daily. Patients were treated for four weeks. The occurrence of ten nasal, eye and throat symptoms was rated (0 = never, 1 = sometimes, 2 = often). All symptoms showed a statistically significant improvement at the final visit, as did the overall sums of the scores. These changes were clinically significant. Overall assessment of efficacy by the physicians and the patients was very good and good in more than 85% of patients. 70% of patients required no concomitant medication. 13.5% of patients experienced adverse events, mostly mild or moderate in severity. Safety and tolerance were assessed as very good and good in more than 97% of cases. No sedation was seen. With respect to both efficacy and safety, there were no differences between patients younger than 6 years and those aged 6-12 years. In conclusion, these results suggest that Allergodil is an effective treatment of the symptoms of allergic rhinitis in children. The subgroup of 48 young patients studied shows that Allergodil was safe and well tolerated in patients aged 2-6 years.

Administration, Intranasal↗