scholarly journals Effect of intravenously injected killed pneumococci on leukocytes, complement, and phagocytosis in rabbits

1980 ◽  
Vol 29 (3) ◽  
pp. 1021-1027
Author(s):  
W P Reed ◽  
P Jaffee ◽  
E L Albright ◽  
R C Williams
Keyword(s):  
Host Defense ◽  
Defense Mechanisms ◽  
Polymorphonuclear Leukocytes ◽  
Pneumococcal Infection ◽  
Pulmonary Involvement ◽  
Colony Forming Units ◽  
Alternate Complement Pathway ◽  
Pneumococcal Serotype ◽  
Circulating Levels ◽  
Complement Pathways

A pneumococcal infection may be lethal in the absence of overwhelming pulmonary involvement, and death may occur even after the organisms have been killed with antibiotics. The mechanism of death is not understood but may be related to circulating pneumococcal products. For investigating the effects of nonviable pneumococci on several host defense mechanisms, rabbits were injected intravenously with 4 X 10(8) colony-forming units of killed sonified type 13 or type 29 pneumococci. Blood was sampled periodically for the next 24 h, and the following were measured: (i) circulating levels of leukocytes; (ii) activity of the classical and alternate complement pathways; and (iii) ability of the serum to opsonize pneumococci for ingestion and killing by polymorphonuclear leukocytes. Saline-injected control rabbits showed no change in any of the functions. Nonimmune rabbits injected with either pneumococcal serotype showed progressive and profound leukopenia, no change or an increase in classical and alternate complement pathway activity, and a profound reduction in the serum-opsonizing capcity for pneumococci of the same serotype as that used in the injection. The opsonizing capacity remained normal for the other serotype. When a previously immunized animal was injected, the opsonizing capacity for the homologous organism remained intact, but leukopenia nervertheless occurred.

scholarly journals Dynamics of Microbial Colonization of the Oral Cavity in Newborns

2013 ◽  
Vol 24 (4) ◽  
pp. 415-419 ◽  
Author(s):  
Paulo Nelson-Filho ◽  
Izabela Goncalves Borba ◽  
Kessia Suenia Fidelis de Mesquita ◽  
Raquel Assed Bezerra Silva ◽  
Alexandra Mussolino de Queiroz ◽  
...  
Keyword(s):  
Oral Cavity ◽  
Host Defense ◽  
Staphylococcus Epidermidis ◽  
Defense Mechanisms ◽  
Mutans Streptococci ◽  
Microbial Colonization ◽  
Oral Microbiota ◽  
Alveolar Process ◽  
Colony Forming Units ◽  
Hygienic Measures

The host defense mechanisms are not well developed in neonates. The aim of this study was to evaluate the dynamics of microbial colonization of the oral cavity in newborns. Eighty-one samples of the oral microbiota were obtained from 51 healthy newborns 10 min to 53 h after birth by gently rubbing sterile swabs onto the surface of the tongue, cheek mucosa, alveolar process and palate. After microbiological processing, counting of the colony forming units of streptococci, staphylococci and Gram-negative aerobic bacilli was performed. Between 10 min and 8 h, Staphylococcus epidermidis was detected in 30.7% of the samples; between 8 and 16 h, S. epidermidis was detected in 69.5% of the samples and streptococci in 56.5% of the samples; between 16 and 24 h, S. epidermidis, streptococci and S. aureus were detected in 77.78%, 85.18% and 37.03% of the samples, respectively. Between 24 and 53 h, S. epidermidis was detected in 88.89%, streptococci in 94.4% and S. aureus in 33.3% of the samples. Mutans streptococci were not detected in any of the samples. The adoption of strict hygienic measures by the mother and the nursing staff should be emphasized to avoid or at least delay the occurrence of infections caused by microorganisms in newborns. In addition, hospital procedures must be aseptic and invasive interventions must be minimized.

Clinical Pharmacology of Antibiotics: Do Antibiotics Interfere with Host/Bacterial Interaction?

1985 ◽  
Vol 6 (8) ◽  
pp. 326-328 ◽  
Author(s):  
Atef M. Shibl
Keyword(s):  
Clinical Pharmacology ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Polymorphonuclear Leukocytes ◽  
Mononuclear Cells ◽  
Antibacterial Action ◽  
Specific Response ◽  
Positive Effects ◽  
Bacterial Interaction ◽  
New Antibiotics

Antibiotics exert a number of effects on bacteria other than simply killing them or inhibiting their growth. Increasing evidence that exposure of bacteria to antibiotics induces profound alterations in the interaction between bacteria and host defense has been noted. The effect of antibiotics on polymorphonuclear leukocytes and the immune specific response of mononuclear cells is reviewed. An understanding of such effects would allow a more rational application of antibiotics, as well as provide direction in the development of new antibiotics that have both specific antibacterial action and positive effects on host defense mechanisms.

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.

Importance of Phosphoinositide 3-Kinase γ in the Host Defense against Pneumococcal Infection

2007 ◽  
Vol 175 (9) ◽  
pp. 958-966 ◽  
Author(s):  
Ulrich A. Maus ◽  
Myriam Backi ◽  
Christine Winter ◽  
Mrigank Srivastava ◽  
Matthias K. Schwarz ◽  
...  
Keyword(s):  
Host Defense ◽  
Pneumococcal Infection ◽  
Phosphoinositide 3 Kinase

scholarly journals Evaluation of a Novel Therapeutic Approach to Treating Severe Pneumococcal Infection Using a Mouse Model

2009 ◽  
Vol 16 (6) ◽  
pp. 806-810 ◽  
Author(s):  
Nikkol Melnick ◽  
Gowrisankar Rajam ◽  
George M. Carlone ◽  
Jacquelyn S. Sampson ◽  
Edwin W. Ades
Keyword(s):  
Single Dose ◽  
Combination Therapy ◽  
Polymorphonuclear Leukocytes ◽  
Low Dose ◽  
Control Level ◽  
Pneumococcal Infection ◽  
Amino Acid Peptide ◽  
Opsonophagocytic Killing

ABSTRACT P4, a 28-amino-acid peptide, is a eukaryotic cellular activator that enhances specific in vitro opsonophagocytic killing of multiple bacterial pathogens. In a previous study, we successfully recreated this phenomenon in mice in vivo by using a two-dose regimen of P4 and pathogen-specific antibodies, which significantly reduced moribundity in mice. For the present study, we hypothesized that the inclusion of a low-dose antibiotic would make it possible to treat the infected mice with a single dose containing a mixture of P4 and a pathogen-specific antibody. A single dose consisting of P4, intravenous immunoglobulin (IVIG), and ceftriaxone effectively reduced moribundity compared to that of untreated controls (n = 10) by 75% (P < 0.05) and rescued all (10 of 10) infected animals (P < 0.05). If rescued animals were reinfected with Streptococcus pneumoniae and treated with a single dose containing P4, IVIG, and ceftriaxone, they could be rerescued. This observation of the repeated successful use of P4 combination therapy demonstrates a low risk of tolerance development. Additionally, we examined the polymorphonuclear leukocytes (PMN) derived from infected mice and observed that P4 enhanced in vitro opsonophagocytic killing (by >80% over the control level; P < 0.05). This finding supports our hypothesis that PMN are activated by P4 during opsonophagocytosis and the recovery of mice from pneumococcal infection. P4 peptide-based combination therapy may offer an alternative and rapid immunotherapy to treat fulminant pneumococcal infection.

Sign in / Sign up

Export Citation Format

Share Document