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How Cytokines Co-occur across Rickettsioses Patients: From Bipartite Visual Analytics to Mechanistic Inferences of a

Suresh K Bhavnani1, Justin Drake, Gowtham Bellala

  • 1Inst. for Translational Sciences, Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX;

AMIA Joint Summits on Translational Science Proceedings. AMIA Joint Summits on Translational Science
|December 5, 2013
PubMed

Insights

Rickettsial diseases like Mediterranean Spotted Fever (MSF) and DEBONEL involve cytokine storms. This study identifies distinct cytokine patterns in MSF patients, suggesting pathways for therapeutic targets.

Area of Science:

  • Infectious Diseases
  • Immunology
  • Molecular Biology

Background:

  • Rickettsial diseases, including Mediterranean Spotted Fever (MSF) and Dermacentor spp.-borne necrosis-erythema lymphadenopathy (DEBONEL), are re-emerging.
  • These infections can cause severe endothelial damage, microvascular leakage, high morbidity, and mortality.
  • The molecular pathways underlying human responses to rickettsiae remain poorly understood.

Purpose of the Study:

  • To analyze co-occurring cytokine profiles in patients with acute localized (DEBONEL) versus systemic (MSF) rickettsiosis.
  • To elucidate the molecular pathways triggered by rickettsial infections in humans.
  • To generate a hypothesis for rickettsia-induced cytokine storm mechanisms and identify potential therapeutic targets.

Main Methods:

  • Bipartite visual analytics were employed to examine cytokine co-occurrence patterns.
  • Candidate cytokines were analyzed in acutely ill patients diagnosed with either MSF or DEBONEL.
  • Patient cytokine expression levels were compared between localized and systemic forms of rickettsiosis.

Main Results:

  • A distinct network core of MSF patients showed high expression of cytokines related to microvascular leakage, endothelial repair, and inflammation.
  • A network periphery comprised both MSF and DEBONEL patients with lower overall cytokine expression.
  • Evidence suggests specific cytokine pathways are activated in systemic rickettsiosis.

Conclusions:

  • The study provides insights into human molecular responses to rickettsial infections.
  • Distinct cytokine profiles differentiate systemic (MSF) from localized (DEBONEL) rickettsiosis.
  • Findings support a hypothesis of rickettsia-induced cytokine storms and highlight potential therapeutic targets.

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