Streptococcus pneumoniae induces mast cell degranulation

Giovanna Barbuti1, Monica Moschioni, Stefano Censini

  • 1Dipartimento di Scienze Biomediche e Oncologia Umana, Sezione di Patologia Generale, Università di Bari, P.zza Giulio Cesare 11, I-70124 Bari, Italy.

Insights

Streptococcus pneumoniae triggers mast cell degranulation, a key innate immune response. This interaction may help the bacteria spread from the respiratory tract without causing inflammation.

Area of Science:

  • Immunology
  • Microbiology
  • Bacterial Pathogenesis

Background:

  • Streptococcus pneumoniae is a common nasopharyngeal colonizer.
  • Pneumococci can cause severe invasive diseases.
  • Mast cells are crucial innate immune cells in respiratory mucosa.

Purpose of the Study:

  • To investigate the interaction between S. pneumoniae and mast cells.
  • To understand the mechanism of mast cell activation by pneumococci.
  • To explore the role of this interaction in bacterial dissemination.

Main Methods:

  • Co-culture of various S. pneumoniae strains with the RBL-2H3 mast cell line.
  • Assessment of mast cell degranulation.
  • Measurement of cytosolic calcium levels.
  • Quantification of TNF-alpha and IL-6 production.

Main Results:

  • Live S. pneumoniae induced dose- and time-dependent mast cell degranulation.
  • Degranulation was partially dependent on cytosolic calcium.
  • No significant production of TNF-alpha or IL-6 was observed.
  • Non-encapsulated strains showed varying degranulation potentials.

Conclusions:

  • S. pneumoniae can induce mast cell degranulation without triggering a major pro-inflammatory cytokine response.
  • This mechanism may facilitate bacterial spread from the respiratory mucosa.
  • Bacterial factors likely mediate degranulation, representing a potential adaptation for host colonization and dissemination.

Related Concept Videos

Inflammation01:38

Inflammation

Overview
Pneumonia I: Introduction01:29

Pneumonia I: Introduction

Pneumonia is an infection of the lower respiratory tract that leads to inflammation of the lung parenchyma, often resulting in the accumulation of inflammatory exudate in the alveoli and airways. Unlike the watery, low-protein fluid exudate in pulmonary edema, the exudate in this case is a thick fluid rich in immune cells, proteins, and debris produced during infection and inflammation.This impairs gas exchange and can lead to consolidation of lung tissue. The infection may be caused by a...
Atypical Pneumonia01:14

Atypical Pneumonia

Atypical pneumonia, often caused by Mycoplasma pneumoniae, is a form of pulmonary infection that differs from the classical presentation of bacterial pneumonia in both its cause and clinical symptoms. Mycoplasma pneumoniae is a pleomorphic bacterium notable for its lack of a rigid cell wall. This structural characteristic imparts resistance to beta-lactam antibiotics and significantly influences the bacterium’s behavior within the human host.Other pathogens responsible for the disease include...
Differentiation of Common Myeloid Progenitor Cells01:15

Differentiation of Common Myeloid Progenitor Cells

Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...
Allergic Reactions02:06

Allergic Reactions

Overview
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...