scholarly journals Subversion of host defense mechanisms by malignant tumors: an established tumor as a privileged site for bacterial growth.

1977 ◽  
Vol 145 (5) ◽  
pp. 1264-1277 ◽  
Author(s):  
G L Spitalny ◽  
R J North
Keyword(s):  
T Cells ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Malignant Tumors ◽  
Activated Macrophages ◽  
Established Tumor ◽  
Hind Foot ◽  
Foot Pad ◽  
Privileged Site ◽  
Contralateral Tumor

Mice carrying any one of three murine tumors in their right hind foot pad were incapable of eliminating an inoculum of the bacterial parasite Listeria monocytogenes from the progressive tumor. In contrast, they were as capable as control mice in efficiently eliminating the organism from their contralateral tumor-free foot pad, and from their lymph nodes and livers. The results serve to show, therefore, that conditions within an established tumor are not only antagonistic to the expression of concomitant anti-tumor immunity, but that they are also antagonistic to the expression of T-cell-mediated anti-bacterial immunity. The possibility was discussed that the tumor contains factors that act pharmacologically to locally suppress the function of sensitized T cells and activated macrophages.

scholarly journals Interleukin-23 (IL-23)-IL-17 Cytokine Axis in Murine Pneumocystis carinii Infection

2007 ◽  
Vol 75 (6) ◽  
pp. 3055-3061 ◽  
Author(s):  
Xiaowen L. Rudner ◽  
Kyle I. Happel ◽  
Erana A. Young ◽  
Judd E. Shellito
Keyword(s):  
T Cells ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Pneumocystis Carinii ◽  
Neutralizing Antibody ◽  
Wild Type ◽  
Pneumocystis Carinii Infection ◽  
Interleukin 23

ABSTRACT Host defense mechanisms against Pneumocystis carinii are not fully understood. Previous work in the murine model has shown that host defense against infection is critically dependent upon host CD4+ T cells. The recently described Th17 immune response is predominantly a function of effector CD4+ T cells stimulated by interleukin-23 (IL-23), but whether these cells are required for defense against P. carinii infection is unknown. We tested the hypothesis that P. carinii stimulates the early release of IL-23, leading to increases in IL-17 production and lung effector CD4+ T-cell population that mediate clearance of infection. In vitro, stimulation of alveolar macrophages with P. carinii induced IL-23, and IL-23p19 mRNA was expressed in lungs of mice infected with this pathogen. To address the role of IL-23 in resistance to P. carinii, IL-23p19−/− and wild-type control C57BL/6 mice were infected and their fungal burdens and cytokine/chemokine responses were compared. IL-23p19−/− mice displayed transient but impaired clearance of infection, which was most apparent 2 weeks after inoculation. In confirmatory studies, the administration of either anti-IL-23p19 or anti-IL-17 neutralizing antibody to wild-type mice infected with P. carinii also caused increases in fungal burdens. IL-17 and the lymphocyte chemokines IP-10, MIG, MIP-1α, MIP-1β, and RANTES were decreased in the lungs of infected IL-23p19−/− mice in comparison to their levels in the lungs of wild-type mice. In IL-23p19−/− mice infected with P. carinii, there were fewer effector CD4+ T cells in the lung tissue. Collectively, these studies indicate that the IL-23-IL-17 axis participates in host defense against P. carinii.

scholarly journals Subversion of host defense mechanisms by murine tumors. II. Counter-influence of concomitant antitumor immunity.

1976 ◽  
Vol 143 (3) ◽  
pp. 574-584 ◽  
Author(s):  
R J North ◽  
D P Kirstein ◽  
R L Tuttle
Keyword(s):  
Tumor Cell ◽  
Host Defense ◽  
Primary Tumor ◽  
Defense Mechanisms ◽  
Antitumor Immunity ◽  
Malignant Tumors ◽  
Acquired Resistance ◽  
Antibacterial Resistance ◽  
Stages Of Growth ◽  
Murine Tumor Cells

Subcutaneous injection of murine tumor cells first resulted in a state of severely suppressed macrophage-mediated antibacterial resistance and then in a contrasting state of greatly enhanced antibacterial resistance. Whereas, the state of suppressed antibacterial resistance corresponded to a state of suppressed resistance to a tumor cell challenge, the generation of enhanced antibacterial resistance corresponded to the acquisition of concomitant antitumor immunity. It was suggested on the basis of this evidence that changes in the level of macrophage-mediated antibacterial resistance that occur during growth of the primary tumor reflected changes in the level of the host's resistance to the tumor itself. It was further suggested that the coincidental suppression of antibacterial and antitumor resistance that occurs during the initial stages of growth of the primary tumor represents the operation of a mechanism that enables the tumor to avoid destruction by macrophages. The results support the view that macrophages play an important role in native and acquired resistance to malignant tumors.

scholarly journals Roles of Activated Macrophages in Host Defense Mechanisms Against Candida Infection.

1997 ◽  
Vol 38 (3) ◽  
pp. 223-227 ◽  
Author(s):  
Shigeru Abe ◽  
Shigeru Tansho ◽  
Katsuhisa Uchida ◽  
Hideyo Yamaguchi
Keyword(s):  
Host Defense ◽  
Defense Mechanisms ◽  
Candida Infection ◽  
Activated Macrophages

Effects of Anesthesia, Surgery and Inflammation Upon Host Defense Mechanisms

1975 ◽  
Vol 48 (5) ◽  
pp. 706-720 ◽  
Author(s):  
M. Schutte ◽  
R. DiCamelli ◽  
P. Murphy ◽  
M. Sadove ◽  
H. Gewurz
Keyword(s):  
Host Defense ◽  
Defense Mechanisms

scholarly journals The History and Mystery of Alveolar Epithelial Type II Cells: Focus on Their Physiologic and Pathologic Role in Lung

2021 ◽  
Vol 22 (5) ◽  
pp. 2566 ◽  
Author(s):  
Barbara Ruaro ◽  
Francesco Salton ◽  
Luca Braga ◽  
Barbara Wade ◽  
Paola Confalonieri ◽  
...  
Keyword(s):  
Host Defense ◽  
Defense Mechanisms ◽  
Work Of Breathing ◽  
Surfactant Proteins ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii ◽  
Lung Protection ◽  
Alveolar Epithelial ◽  
Distal Lung

Alveolar type II (ATII) cells are a key structure of the distal lung epithelium, where they exert their innate immune response and serve as progenitors of alveolar type I (ATI) cells, contributing to alveolar epithelial repair and regeneration. In the healthy lung, ATII cells coordinate the host defense mechanisms, not only generating a restrictive alveolar epithelial barrier, but also orchestrating host defense mechanisms and secreting surfactant proteins, which are important in lung protection against pathogen exposure. Moreover, surfactant proteins help to maintain homeostasis in the distal lung and reduce surface tension at the pulmonary air–liquid interface, thereby preventing atelectasis and reducing the work of breathing. ATII cells may also contribute to the fibroproliferative reaction by secreting growth factors and proinflammatory molecules after damage. Indeed, various acute and chronic diseases are associated with intensive inflammation. These include oedema, acute respiratory distress syndrome, fibrosis and numerous interstitial lung diseases, and are characterized by hyperplastic ATII cells which are considered an essential part of the epithelialization process and, consequently, wound healing. The aim of this review is that of revising the physiologic and pathologic role ATII cells play in pulmonary diseases, as, despite what has been learnt in the last few decades of research, the origin, phenotypic regulation and crosstalk of these cells still remain, in part, a mystery.

scholarly journals Role of Intestinal Mucins in Innate Host Defense Mechanisms against Pathogens

2008 ◽  
Vol 1 (2) ◽  
pp. 123-135 ◽  
Author(s):  
Poonam Dharmani ◽  
Vikas Srivastava ◽  
Vanessa Kissoon-Singh ◽  
Kris Chadee
Keyword(s):  
Host Defense ◽  
Defense Mechanisms ◽  
Intestinal Mucins
Sign in / Sign up

Export Citation Format

Share Document